Alzheimer's & Cognition

In the case of a hip fracture, operating on a patient with dementia can be a difficult decision to make. Indeed, surgery exposes patients with dementia to a higher mortality rate, more delirium and postoperative complications, and a greater loss of mobility than patients of the same age without cognitive impairments. For patients with dementia in institutional settings, survival is better for those who undergo surgery than for those who do not. But what about the prognosis of surgery vs no surgery for patients with dementia who live at home?

To answer this question, researchers in the United States conducted a cohort study using Medicare data. This retrospective study included patients aged 66 years and older with dementia who were living at home and not placed in institutions and who had a hip fracture between January 2017 and June 2018. Patients with incomplete observations, particularly regarding the location and type of residence (home/institution), were excluded from the analysis. Fractures were categorized as (i) fractures of the head and neck, (ii) pertrochanteric, (iii) subtrochanteric, and (iv) multiple/complex. The type and severity (mild, moderate, or severe) of dementia were identified using the diagnostic code list in the International Statistical Classification of Diseases, Tenth Revision.
 

Examining Mortality

The primary outcome was mortality at 30, 90, and 180 days. Secondary outcomes included hospital delirium; the need for subsequent hospitalization (within 6 months) or home health services (within 10 days); and intensive care interventions such as dialysis, intubation, resuscitation maneuvers, mechanical ventilation, or the insertion of a feeding tube.

Postoperative medical facility admissions were distinguished according to whether there was a plan to return home. To compare the surgery and nonsurgery groups, an inverse propensity score analysis was conducted within subgroups determined by fracture type, comorbidities (using the Elixhauser score), the person or entity responsible for admission (ie, physician, clinic, hospital, etc.), dual eligibility (Medicare and Medicaid), place of residence (ie, urban or rural), race, and sex. Dementia severity was estimated using a frailty index on the basis of evaluation tests that were systematically collected in the Medicare database.
 

Results Favored Surgery

Among 56,209 patients with dementia who were admitted for a hip fracture (73.0% women; mean age, 86.4 ± 7.0 years), 33,142 (59.0%) underwent surgery and 23,067 (41.0%) did not. Among surgically treated patients, 73.3% had fractures of the head or neck of the femur, and 40.2% had moderate to severe dementia. The nonsurgically treated fractures were 78.5% pertrochanteric. Comorbidities were evenly distributed between the two groups.

At 180 days, mortality was 31.8% in the surgery group compared with 45.7% in the nonsurgery group, resulting in a significant reduction in the unadjusted relative risk (RR) for death in favor of surgery (RR, 0.67; 95% CI, 0.60-0.76; P < .001). Among patients with mild dementia and a fracture of the head or neck of the femur, mortality at 180 days was 26.5% among surgical patients and 34.9% among nonsurgical patients (RR, 0.67; 95% CI, 0.60-0.76; P < .001). After the investigators adjusted for risk according to propensity score, the benefit of surgery remained significant at 30, 90, and 180 days, regardless of dementia severity. There was no significant difference in mortality for other types of hip fractures between the surgery and nonsurgery groups, however.

The adjusted RR for in-hospital delirium was 1.23 (P = .008), which was significant for the surgery group, but only for those with moderate to severe dementia. There were also fewer permanent placements (P < .001) among the surgically treated patients, and fewer patients with mild dementia required nurse care at home. There was no difference in resuscitation maneuvers between surgery and nonsurgery patients, whether the dementia was mild or not. For patients with a fracture of the head or neck of the femur, there was no difference in the likelihood of rehabilitation admission within 180 days, whether they were operated on or not.
 

Ethical Considerations

This study can inform discussions among healthcare professionals, patients, and patients’ families about which goals to set and which strategy to choose. The main interest of this study lies in its comparison of outcomes between patients with dementia who were operated on and those who were not, rather than comparing patients with and without dementia. Among patients with dementia living at home with a fracture of the head or neck of the femur, those who underwent surgery had a lower risk for death than those who did not, regardless of the severity of dementia.

It is noteworthy that less than two thirds of patients with dementia underwent surgery, which contradicts recommendations for almost routine surgery for patients with dementia. This observation raises questions about respecting patient wishes and advance directives when known, possible detrimental delays in referrals, and legal-medical issues.

Furthermore, the treatment choices of American surgeons are clearly influenced by the type of hip fracture. Fractures of the head and neck of the femur are typically treated with prosthetic arthroplasty, which simplifies postoperative care, compared with osteosynthesis. The latter procedure is more often used for extra-articular hip fractures but entails higher risks. While survival is an apparently more easily achievable goal through surgery, ethical considerations about other treatment objectives such as pain control, functional recovery, and treatment adequacy cannot be overlooked. It is worth noting that the French National Authority for Health issued recommendations in 2018 regarding the care pathway for patients hospitalized for a hip fracture within an orthogeriatric organization.

This story was translated from JIM, which is part of the Medscape Medical News professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

In the case of a hip fracture, operating on a patient with dementia can be a difficult decision to make. Indeed, surgery exposes patients with dementia to a higher mortality rate, more delirium and postoperative complications, and a greater loss of mobility than patients of the same age without cognitive impairments. For patients with dementia in institutional settings, survival is better for those who undergo surgery than for those who do not. But what about the prognosis of surgery vs no surgery for patients with dementia who live at home?

To answer this question, researchers in the United States conducted a cohort study using Medicare data. This retrospective study included patients aged 66 years and older with dementia who were living at home and not placed in institutions and who had a hip fracture between January 2017 and June 2018. Patients with incomplete observations, particularly regarding the location and type of residence (home/institution), were excluded from the analysis. Fractures were categorized as (i) fractures of the head and neck, (ii) pertrochanteric, (iii) subtrochanteric, and (iv) multiple/complex. The type and severity (mild, moderate, or severe) of dementia were identified using the diagnostic code list in the International Statistical Classification of Diseases, Tenth Revision.
 

Examining Mortality

The primary outcome was mortality at 30, 90, and 180 days. Secondary outcomes included hospital delirium; the need for subsequent hospitalization (within 6 months) or home health services (within 10 days); and intensive care interventions such as dialysis, intubation, resuscitation maneuvers, mechanical ventilation, or the insertion of a feeding tube.

Postoperative medical facility admissions were distinguished according to whether there was a plan to return home. To compare the surgery and nonsurgery groups, an inverse propensity score analysis was conducted within subgroups determined by fracture type, comorbidities (using the Elixhauser score), the person or entity responsible for admission (ie, physician, clinic, hospital, etc.), dual eligibility (Medicare and Medicaid), place of residence (ie, urban or rural), race, and sex. Dementia severity was estimated using a frailty index on the basis of evaluation tests that were systematically collected in the Medicare database.
 

Results Favored Surgery

Among 56,209 patients with dementia who were admitted for a hip fracture (73.0% women; mean age, 86.4 ± 7.0 years), 33,142 (59.0%) underwent surgery and 23,067 (41.0%) did not. Among surgically treated patients, 73.3% had fractures of the head or neck of the femur, and 40.2% had moderate to severe dementia. The nonsurgically treated fractures were 78.5% pertrochanteric. Comorbidities were evenly distributed between the two groups.

At 180 days, mortality was 31.8% in the surgery group compared with 45.7% in the nonsurgery group, resulting in a significant reduction in the unadjusted relative risk (RR) for death in favor of surgery (RR, 0.67; 95% CI, 0.60-0.76; P < .001). Among patients with mild dementia and a fracture of the head or neck of the femur, mortality at 180 days was 26.5% among surgical patients and 34.9% among nonsurgical patients (RR, 0.67; 95% CI, 0.60-0.76; P < .001). After the investigators adjusted for risk according to propensity score, the benefit of surgery remained significant at 30, 90, and 180 days, regardless of dementia severity. There was no significant difference in mortality for other types of hip fractures between the surgery and nonsurgery groups, however.

The adjusted RR for in-hospital delirium was 1.23 (P = .008), which was significant for the surgery group, but only for those with moderate to severe dementia. There were also fewer permanent placements (P < .001) among the surgically treated patients, and fewer patients with mild dementia required nurse care at home. There was no difference in resuscitation maneuvers between surgery and nonsurgery patients, whether the dementia was mild or not. For patients with a fracture of the head or neck of the femur, there was no difference in the likelihood of rehabilitation admission within 180 days, whether they were operated on or not.
 

Ethical Considerations

This study can inform discussions among healthcare professionals, patients, and patients’ families about which goals to set and which strategy to choose. The main interest of this study lies in its comparison of outcomes between patients with dementia who were operated on and those who were not, rather than comparing patients with and without dementia. Among patients with dementia living at home with a fracture of the head or neck of the femur, those who underwent surgery had a lower risk for death than those who did not, regardless of the severity of dementia.

It is noteworthy that less than two thirds of patients with dementia underwent surgery, which contradicts recommendations for almost routine surgery for patients with dementia. This observation raises questions about respecting patient wishes and advance directives when known, possible detrimental delays in referrals, and legal-medical issues.

Furthermore, the treatment choices of American surgeons are clearly influenced by the type of hip fracture. Fractures of the head and neck of the femur are typically treated with prosthetic arthroplasty, which simplifies postoperative care, compared with osteosynthesis. The latter procedure is more often used for extra-articular hip fractures but entails higher risks. While survival is an apparently more easily achievable goal through surgery, ethical considerations about other treatment objectives such as pain control, functional recovery, and treatment adequacy cannot be overlooked. It is worth noting that the French National Authority for Health issued recommendations in 2018 regarding the care pathway for patients hospitalized for a hip fracture within an orthogeriatric organization.

This story was translated from JIM, which is part of the Medscape Medical News professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

In the case of a hip fracture, operating on a patient with dementia can be a difficult decision to make. Indeed, surgery exposes patients with dementia to a higher mortality rate, more delirium and postoperative complications, and a greater loss of mobility than patients of the same age without cognitive impairments. For patients with dementia in institutional settings, survival is better for those who undergo surgery than for those who do not. But what about the prognosis of surgery vs no surgery for patients with dementia who live at home?

To answer this question, researchers in the United States conducted a cohort study using Medicare data. This retrospective study included patients aged 66 years and older with dementia who were living at home and not placed in institutions and who had a hip fracture between January 2017 and June 2018. Patients with incomplete observations, particularly regarding the location and type of residence (home/institution), were excluded from the analysis. Fractures were categorized as (i) fractures of the head and neck, (ii) pertrochanteric, (iii) subtrochanteric, and (iv) multiple/complex. The type and severity (mild, moderate, or severe) of dementia were identified using the diagnostic code list in the International Statistical Classification of Diseases, Tenth Revision.
 

Examining Mortality

The primary outcome was mortality at 30, 90, and 180 days. Secondary outcomes included hospital delirium; the need for subsequent hospitalization (within 6 months) or home health services (within 10 days); and intensive care interventions such as dialysis, intubation, resuscitation maneuvers, mechanical ventilation, or the insertion of a feeding tube.

Postoperative medical facility admissions were distinguished according to whether there was a plan to return home. To compare the surgery and nonsurgery groups, an inverse propensity score analysis was conducted within subgroups determined by fracture type, comorbidities (using the Elixhauser score), the person or entity responsible for admission (ie, physician, clinic, hospital, etc.), dual eligibility (Medicare and Medicaid), place of residence (ie, urban or rural), race, and sex. Dementia severity was estimated using a frailty index on the basis of evaluation tests that were systematically collected in the Medicare database.
 

Results Favored Surgery

Among 56,209 patients with dementia who were admitted for a hip fracture (73.0% women; mean age, 86.4 ± 7.0 years), 33,142 (59.0%) underwent surgery and 23,067 (41.0%) did not. Among surgically treated patients, 73.3% had fractures of the head or neck of the femur, and 40.2% had moderate to severe dementia. The nonsurgically treated fractures were 78.5% pertrochanteric. Comorbidities were evenly distributed between the two groups.

At 180 days, mortality was 31.8% in the surgery group compared with 45.7% in the nonsurgery group, resulting in a significant reduction in the unadjusted relative risk (RR) for death in favor of surgery (RR, 0.67; 95% CI, 0.60-0.76; P < .001). Among patients with mild dementia and a fracture of the head or neck of the femur, mortality at 180 days was 26.5% among surgical patients and 34.9% among nonsurgical patients (RR, 0.67; 95% CI, 0.60-0.76; P < .001). After the investigators adjusted for risk according to propensity score, the benefit of surgery remained significant at 30, 90, and 180 days, regardless of dementia severity. There was no significant difference in mortality for other types of hip fractures between the surgery and nonsurgery groups, however.

The adjusted RR for in-hospital delirium was 1.23 (P = .008), which was significant for the surgery group, but only for those with moderate to severe dementia. There were also fewer permanent placements (P < .001) among the surgically treated patients, and fewer patients with mild dementia required nurse care at home. There was no difference in resuscitation maneuvers between surgery and nonsurgery patients, whether the dementia was mild or not. For patients with a fracture of the head or neck of the femur, there was no difference in the likelihood of rehabilitation admission within 180 days, whether they were operated on or not.
 

Ethical Considerations

This study can inform discussions among healthcare professionals, patients, and patients’ families about which goals to set and which strategy to choose. The main interest of this study lies in its comparison of outcomes between patients with dementia who were operated on and those who were not, rather than comparing patients with and without dementia. Among patients with dementia living at home with a fracture of the head or neck of the femur, those who underwent surgery had a lower risk for death than those who did not, regardless of the severity of dementia.

It is noteworthy that less than two thirds of patients with dementia underwent surgery, which contradicts recommendations for almost routine surgery for patients with dementia. This observation raises questions about respecting patient wishes and advance directives when known, possible detrimental delays in referrals, and legal-medical issues.

Furthermore, the treatment choices of American surgeons are clearly influenced by the type of hip fracture. Fractures of the head and neck of the femur are typically treated with prosthetic arthroplasty, which simplifies postoperative care, compared with osteosynthesis. The latter procedure is more often used for extra-articular hip fractures but entails higher risks. While survival is an apparently more easily achievable goal through surgery, ethical considerations about other treatment objectives such as pain control, functional recovery, and treatment adequacy cannot be overlooked. It is worth noting that the French National Authority for Health issued recommendations in 2018 regarding the care pathway for patients hospitalized for a hip fracture within an orthogeriatric organization.

This story was translated from JIM, which is part of the Medscape Medical News professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

In 2019, 57 million people worldwide were living with dementia, a figure expected to soar to 153 million by 2050. A recent Lancet Commission report suggests that nearly half of dementia cases could be prevented or delayed by addressing 14 modifiable risk factors, including impaired vision. 

The report’s authors recommend that vision-loss screening and treatment be universally available. But are these recommendations warranted? What is the evidence? What is the potential mechanism? And what are the potential implications for clinical practice? 

Worldwide, the prevalence of avoidable vision loss and blindness in adults aged 50 years or older is estimated to hover around 13%.

“There is now overwhelming evidence that vision impairment in later life is associated with more rapid cognitive decline and an increased risk of dementia,” said Joshua Ehrlich, MD, MPH, associate professor in ophthalmology and visual sciences, the Institute for Social Research at the University of Michigan, Ann Arbor. 

The evidence includes a meta-analysis of 14 prospective cohort studies with roughly 6.2 million older adults who were cognitively intact at baseline. Over the course of up to 14 years, 171,888 developed dementia. Vision loss was associated with a pooled relative risk (RR) for dementia of 1.47. 

A separate meta-analysis also identified an increased risk for dementia (RR, 1.38) with visual loss. When broken down into different eye conditions, an increased dementia risk was associated with cataracts and diabetic retinopathy but not with glaucoma or age-related macular degeneration.

A US study that followed roughly 3000 older adults with cataracts and normal cognition at baseline for more than 20 years found that those who had cataract extraction had significantly reduced risk for dementia compared with those who did not have cataract extraction (hazard ratio, 0.71), after controlling for age, race, APOE genotype, education, smoking, and an extensive list of comorbidities. 
 

Causation or Coincidence?

The mechanisms behind these associations might be related to underlying illness, such as diabetes, which is a risk factor for dementia; vision loss itself, as might be suggested by a possible effect of cataract surgery; or shared neuropathologic processes in the retina and the brain. 

A longitudinal study from Korea that included roughly 6 million adults showed that dementia risk increased with severity of visual loss, which supports the hypothesis that vision loss in itself might be causal or that there is a dose-response effect to a shared causal factor. 

“Work is still needed to sort out” exactly how visual deficits may raise dementia risk, although several hypotheses exist, Dr. Ehrlich said. 

For example, “decreased input to the brain via the visual pathways may directly induce brain changes. Also, consequences of vision loss, like social isolation, physical inactivity, and depression, are themselves risk factors for dementia and may explain the pathways through which vision impairment increases risk,” he said. 

Is the link causal? “We’ll never know definitively because we can’t randomize people to not get cataract surgery versus getting cataract surgery, because we know that improving vision improves quality of life, so we’d never want to do that. But the new evidence that’s come in over the last 5 years or so is pretty promising,” said Esme Fuller-Thomson, PhD, director of the Institute for Life Course and Aging and professor, Department of Family and Community Medicine and Faculty of Nursing, at the University of Toronto, Ontario, Canada.

She noted that results of two studies that have looked at this “seem to indicate that those who have cataract surgery are not nearly at as high risk of dementia as those who have cataracts but don’t have the surgery. That’s leaning towards causality.”

A study published in July suggests that cataracts increase dementia risk through vascular and non–Alzheimer’s disease mechanisms. 
 

Clear Clinical Implications 

Dr. Ehrlich said that evidence for an association between untreated vision loss and dementia risk and potential modification by treatment has clear implications for care. 

“Loss of vision impacts so many aspects of people’s lives beyond just how they see the world and losing vision in later life is not a normal part of aging. Thus, when older adults experience vision loss, this should be a cause for concern and prompt an immediate referral to an eye care professional,” he noted. 

Dr. Fuller-Thomson agrees. “Addressing vision loss will certainly help people see better and function at a higher level and improve quality of life, and it seems probable that it might decrease dementia risk so it’s a win-win,” she said.

In her own research, Dr. Fuller-Thomson has found that the combination of hearing loss and vision loss is linked to an eightfold increased risk for cognitive impairment.

“The idea is that vision and/or hearing loss makes it harder for you to be physically active, to be socially engaged, to be mentally stimulated. They are equally important in terms of social isolation, which could lead to loneliness, and we know that loneliness is not good for dementia,” she said.

“With dual sensory impairment, you don’t have as much information coming in — your brain is not engaged as much — and having an engaged brain, doing hobbies, having intellectually stimulating conversation, all of those are factors are associated with lowering risk of dementia,” Dr. Fuller-Thomson said.

The latest Lancet Commission report noted that treatment for visual loss is “effective and cost-effective” for an estimated 90% of people. However, across the world, particularly in low- and middle-income countries, visual loss often goes untreated. 

“A clear opportunity for dementia prevention exists with treatment of visual loss,” the report concluded.

Dr. Ehrlich and Dr. Fuller-Thomson have no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

In 2019, 57 million people worldwide were living with dementia, a figure expected to soar to 153 million by 2050. A recent Lancet Commission report suggests that nearly half of dementia cases could be prevented or delayed by addressing 14 modifiable risk factors, including impaired vision. 

The report’s authors recommend that vision-loss screening and treatment be universally available. But are these recommendations warranted? What is the evidence? What is the potential mechanism? And what are the potential implications for clinical practice? 

Worldwide, the prevalence of avoidable vision loss and blindness in adults aged 50 years or older is estimated to hover around 13%.

“There is now overwhelming evidence that vision impairment in later life is associated with more rapid cognitive decline and an increased risk of dementia,” said Joshua Ehrlich, MD, MPH, associate professor in ophthalmology and visual sciences, the Institute for Social Research at the University of Michigan, Ann Arbor. 

The evidence includes a meta-analysis of 14 prospective cohort studies with roughly 6.2 million older adults who were cognitively intact at baseline. Over the course of up to 14 years, 171,888 developed dementia. Vision loss was associated with a pooled relative risk (RR) for dementia of 1.47. 

A separate meta-analysis also identified an increased risk for dementia (RR, 1.38) with visual loss. When broken down into different eye conditions, an increased dementia risk was associated with cataracts and diabetic retinopathy but not with glaucoma or age-related macular degeneration.

A US study that followed roughly 3000 older adults with cataracts and normal cognition at baseline for more than 20 years found that those who had cataract extraction had significantly reduced risk for dementia compared with those who did not have cataract extraction (hazard ratio, 0.71), after controlling for age, race, APOE genotype, education, smoking, and an extensive list of comorbidities. 
 

Causation or Coincidence?

The mechanisms behind these associations might be related to underlying illness, such as diabetes, which is a risk factor for dementia; vision loss itself, as might be suggested by a possible effect of cataract surgery; or shared neuropathologic processes in the retina and the brain. 

A longitudinal study from Korea that included roughly 6 million adults showed that dementia risk increased with severity of visual loss, which supports the hypothesis that vision loss in itself might be causal or that there is a dose-response effect to a shared causal factor. 

“Work is still needed to sort out” exactly how visual deficits may raise dementia risk, although several hypotheses exist, Dr. Ehrlich said. 

For example, “decreased input to the brain via the visual pathways may directly induce brain changes. Also, consequences of vision loss, like social isolation, physical inactivity, and depression, are themselves risk factors for dementia and may explain the pathways through which vision impairment increases risk,” he said. 

Is the link causal? “We’ll never know definitively because we can’t randomize people to not get cataract surgery versus getting cataract surgery, because we know that improving vision improves quality of life, so we’d never want to do that. But the new evidence that’s come in over the last 5 years or so is pretty promising,” said Esme Fuller-Thomson, PhD, director of the Institute for Life Course and Aging and professor, Department of Family and Community Medicine and Faculty of Nursing, at the University of Toronto, Ontario, Canada.

She noted that results of two studies that have looked at this “seem to indicate that those who have cataract surgery are not nearly at as high risk of dementia as those who have cataracts but don’t have the surgery. That’s leaning towards causality.”

A study published in July suggests that cataracts increase dementia risk through vascular and non–Alzheimer’s disease mechanisms. 
 

Clear Clinical Implications 

Dr. Ehrlich said that evidence for an association between untreated vision loss and dementia risk and potential modification by treatment has clear implications for care. 

“Loss of vision impacts so many aspects of people’s lives beyond just how they see the world and losing vision in later life is not a normal part of aging. Thus, when older adults experience vision loss, this should be a cause for concern and prompt an immediate referral to an eye care professional,” he noted. 

Dr. Fuller-Thomson agrees. “Addressing vision loss will certainly help people see better and function at a higher level and improve quality of life, and it seems probable that it might decrease dementia risk so it’s a win-win,” she said.

In her own research, Dr. Fuller-Thomson has found that the combination of hearing loss and vision loss is linked to an eightfold increased risk for cognitive impairment.

“The idea is that vision and/or hearing loss makes it harder for you to be physically active, to be socially engaged, to be mentally stimulated. They are equally important in terms of social isolation, which could lead to loneliness, and we know that loneliness is not good for dementia,” she said.

“With dual sensory impairment, you don’t have as much information coming in — your brain is not engaged as much — and having an engaged brain, doing hobbies, having intellectually stimulating conversation, all of those are factors are associated with lowering risk of dementia,” Dr. Fuller-Thomson said.

The latest Lancet Commission report noted that treatment for visual loss is “effective and cost-effective” for an estimated 90% of people. However, across the world, particularly in low- and middle-income countries, visual loss often goes untreated. 

“A clear opportunity for dementia prevention exists with treatment of visual loss,” the report concluded.

Dr. Ehrlich and Dr. Fuller-Thomson have no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

In 2019, 57 million people worldwide were living with dementia, a figure expected to soar to 153 million by 2050. A recent Lancet Commission report suggests that nearly half of dementia cases could be prevented or delayed by addressing 14 modifiable risk factors, including impaired vision. 

The report’s authors recommend that vision-loss screening and treatment be universally available. But are these recommendations warranted? What is the evidence? What is the potential mechanism? And what are the potential implications for clinical practice? 

Worldwide, the prevalence of avoidable vision loss and blindness in adults aged 50 years or older is estimated to hover around 13%.

“There is now overwhelming evidence that vision impairment in later life is associated with more rapid cognitive decline and an increased risk of dementia,” said Joshua Ehrlich, MD, MPH, associate professor in ophthalmology and visual sciences, the Institute for Social Research at the University of Michigan, Ann Arbor. 

The evidence includes a meta-analysis of 14 prospective cohort studies with roughly 6.2 million older adults who were cognitively intact at baseline. Over the course of up to 14 years, 171,888 developed dementia. Vision loss was associated with a pooled relative risk (RR) for dementia of 1.47. 

A separate meta-analysis also identified an increased risk for dementia (RR, 1.38) with visual loss. When broken down into different eye conditions, an increased dementia risk was associated with cataracts and diabetic retinopathy but not with glaucoma or age-related macular degeneration.

A US study that followed roughly 3000 older adults with cataracts and normal cognition at baseline for more than 20 years found that those who had cataract extraction had significantly reduced risk for dementia compared with those who did not have cataract extraction (hazard ratio, 0.71), after controlling for age, race, APOE genotype, education, smoking, and an extensive list of comorbidities. 
 

Causation or Coincidence?

The mechanisms behind these associations might be related to underlying illness, such as diabetes, which is a risk factor for dementia; vision loss itself, as might be suggested by a possible effect of cataract surgery; or shared neuropathologic processes in the retina and the brain. 

A longitudinal study from Korea that included roughly 6 million adults showed that dementia risk increased with severity of visual loss, which supports the hypothesis that vision loss in itself might be causal or that there is a dose-response effect to a shared causal factor. 

“Work is still needed to sort out” exactly how visual deficits may raise dementia risk, although several hypotheses exist, Dr. Ehrlich said. 

For example, “decreased input to the brain via the visual pathways may directly induce brain changes. Also, consequences of vision loss, like social isolation, physical inactivity, and depression, are themselves risk factors for dementia and may explain the pathways through which vision impairment increases risk,” he said. 

Is the link causal? “We’ll never know definitively because we can’t randomize people to not get cataract surgery versus getting cataract surgery, because we know that improving vision improves quality of life, so we’d never want to do that. But the new evidence that’s come in over the last 5 years or so is pretty promising,” said Esme Fuller-Thomson, PhD, director of the Institute for Life Course and Aging and professor, Department of Family and Community Medicine and Faculty of Nursing, at the University of Toronto, Ontario, Canada.

She noted that results of two studies that have looked at this “seem to indicate that those who have cataract surgery are not nearly at as high risk of dementia as those who have cataracts but don’t have the surgery. That’s leaning towards causality.”

A study published in July suggests that cataracts increase dementia risk through vascular and non–Alzheimer’s disease mechanisms. 
 

Clear Clinical Implications 

Dr. Ehrlich said that evidence for an association between untreated vision loss and dementia risk and potential modification by treatment has clear implications for care. 

“Loss of vision impacts so many aspects of people’s lives beyond just how they see the world and losing vision in later life is not a normal part of aging. Thus, when older adults experience vision loss, this should be a cause for concern and prompt an immediate referral to an eye care professional,” he noted. 

Dr. Fuller-Thomson agrees. “Addressing vision loss will certainly help people see better and function at a higher level and improve quality of life, and it seems probable that it might decrease dementia risk so it’s a win-win,” she said.

In her own research, Dr. Fuller-Thomson has found that the combination of hearing loss and vision loss is linked to an eightfold increased risk for cognitive impairment.

“The idea is that vision and/or hearing loss makes it harder for you to be physically active, to be socially engaged, to be mentally stimulated. They are equally important in terms of social isolation, which could lead to loneliness, and we know that loneliness is not good for dementia,” she said.

“With dual sensory impairment, you don’t have as much information coming in — your brain is not engaged as much — and having an engaged brain, doing hobbies, having intellectually stimulating conversation, all of those are factors are associated with lowering risk of dementia,” Dr. Fuller-Thomson said.

The latest Lancet Commission report noted that treatment for visual loss is “effective and cost-effective” for an estimated 90% of people. However, across the world, particularly in low- and middle-income countries, visual loss often goes untreated. 

“A clear opportunity for dementia prevention exists with treatment of visual loss,” the report concluded.

Dr. Ehrlich and Dr. Fuller-Thomson have no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

At least 25% of unresponsive patients with a disorder of consciousness show signs of brain activity, an estimate that is higher than previous studies suggest.

“We found that at least 1 in 4 patients who are unresponsive to commands might actually be quite present and highly cognitive,” said study investigator Nicholas D. Schiff, MD, Feil Family Brain & Mind Research Institute and Department of Neurology, Weill Cornell Medicine, Rockefeller University Hospital, New York.

“In other words, if you go to the bedside and carefully examine someone with a severe brain injury and find no evidence of responsiveness, no one has been able to give you an a priori number to say how likely you are to be wrong in thinking this person is actually unaware, not processing language, and not capable of high-level cognitive work. And the answer to that now is at least 1 in 4 times.”

The findings were published online in The New England Journal of Medicine.
 

Clinical Implications? 

Cognitive motor dissociation (CMD) is a condition whereby patients with a severe brain injury who are unresponsive to commands at the bedside show brain activity on functional MRI (fMRI) or electroencephalography (EEG) when presented with selective motor imagery commands, such as “imagine playing tennis,” or “ imagine opening and closing your hand.”

Previous research shows that CMD is present in 10%-20% of people with a disorder of consciousness, a rate similar to that in patients with acute or chronic brain injury.

Understanding that a patient who appears unconscious has signs of cognitive processing could change the way clinicians and family interact with such individuals. Unresponsive patients who are aware may eventually be able to harness emerging communication technologies such as brain-computer interfaces.

In addition, knowing an individual’s CMD status could aid in prognosis. “We know from one study that there’s a four times increased likelihood that patients will be independent in a year in their function if they have cognitive motor dissociation,” said Dr. Schiff.

Unlike most previous studies of CMD, which were conducted at single sites and had relatively small cohorts, this new study included 353 adults with a disorder of consciousness (mean age, 37.9 years; 64% male) at six multinational sites.

Participants were recruited using a variety of methods, including consecutive enrollment of critically ill patients in the intensive care unit and enrollment of those with chronic illness or injury who were in the postacute phase of brain injury.
 

Response to Commands

Study participants were at different stages of recovery from an acute brain injury that had occurred an average of 8 months before the study started.

To determine the presence or absence of an observable response to commands among participants, trained staff used the Coma Recovery Scale–Revised (CRS-R); scores on this instrument range from 0 to 23, and higher scores indicate better neurobehavioral function.

About 40% of individuals were diagnosed with coma or vegetative state, 29% with minimally conscious state–minus, and 22% with minimally conscious state–plus. In all, 10% had emerged from a minimally conscious state.

Researchers assessed response to timed and repeated commands using fMRI or EEG in participants without an observable response to verbal commands, including those with a behavioral diagnosis of coma, vegetative state, or minimally conscious state–minus, and in participants with an observable response to verbal commands.

Of the 353 study participants, 61% underwent at least one fMRI assessment and 74% at least one EEG assessment. Both fMRI and EEG were performed in 35% of participants.

Dr. Schiff explained the two assessment types provide slightly different information, in that they measuring different types of brain signals. He also noted that although “every medical center in the world” has EEG, many do not have fMRI.

The brain imaging assessments captured brain activity within the motor area of the frontal cortex when tasked with motor imagery.

Of the 241 participants deemed to be in a coma or vegetative state or minimally conscious state–minus on the basis of CRS-R score, 60 (25%) had a response to commands on task-based fMRI, task-based EEG, or both.

The percentage of participants with CMD varied across study sites, from 2% to 45%, but Dr. Schiff said the reason for this is unclear. 

The proportion of participants with CMD may have been even higher if all individuals had been assessed with both imaging techniques, he said.
 

Higher Rate of Awareness Than in Previous Research

The investigators noted that the percentage of participants with CMD in their study was up to 10 percentage points higher than in previous studies. This may be due to the multimodal approach that classified participants undergoing assessment with both fMRI and EEG on the basis of responses on either technique, they said. 

The median age was lower among participants with CMD than those without CMD (30.5 years vs 45.3 years).

Compared with participants without CMD, a higher percentage of those with such dissociation had brain trauma as an etiologic factor (65% vs 38%) and a diagnosis of minimally conscious state–minus on the CRS-R (53% vs 38%).

Among people with CMD, 18% were assessed with fMRI only, 22% with EEG only, and 60% with both fMRI and EEG.

Dr. Schiff noted that the use of both fMRI and EEG appears to be more sensitive in detecting brain activity during tasks compared with use of one of these techniques alone.

Of the 112 participants with a diagnosis of minimally conscious state–plus or who had emerged from the minimally conscious state, 38% had a response to commands on task-based fMRI, task-based EEG, or both. Among these participants, 23% were assessed with fMRI only, 19% with EEG only, and 58% with both fMRI and EEG.

Research shows “it’s very clear that people with severe brain injury continue to get better over time,” noted Dr. Schiff. “Every month and week matters, and so it probably is the case that a lot of these patients are picking up the level of recovery, and the later we go out to measure them, the more likely we are to find people who are CMD than not.”

These new results should prompt further study to explore whether detection of CMD can lead to improved outcomes, the investigators noted. “In addition, the standardization, validation, and simplification of task-based fMRI and EEG methods that are used to detect cognitive motor dissociation are needed to prompt widespread clinical integration of these techniques and investigation of the bioethical implications of the findings.”

All study participants with chronic brain injury had survived their initial illness or injury and had access to a research facility with advanced fMRI and EEG capabilities. “This survival bias may reflect greater cognitive reserve and resilience over time among the participants. As such, the results of our study may not be generalizable to the overall population of patients with cognitive motor dissociation,” the investigators wrote.

Another study limitation was that participating sites used heterogeneous strategies to acquire, analyze, and interpret data, which led to differences in the number, type, and ordering of the cognitive tasks assessed on fMRI and EEG.

“These differences, along with variations in recruitment strategies and participant characteristics, may have contributed to the unequal percentage of participants with cognitive motor dissociation observed at each site. Our findings may therefore not be generalizable across all centers,” the researchers wrote. 

Only a few academic medical centers have the specially trained personnel and techniques needed to assess patients for CMD — which, the researchers noted, limits the feasibility of performing these assessments in general practice.
 

Challenging Research

Commenting on the research, Aarti Sarwal, MD, professor of neurology and section chief, Neurocritical Care, Virginia Commonwealth University, Richmond, Virginia, noted that this was a “very challenging” study to perform, given that only a few academic centers are equipped to perform both fMRI and quantitative EEG analysis.

“In general, finding patients this far out, who have access to clinical, radiological, and electrophysiological testing and were provided good care enough to receive these, is a mammoth task in itself.” 

Dr. Sarwal said the study builds on efforts of the Curing Coma campaign , a clinical, scientific, and public health effort of the Neurocritical Care Society to tackle the concept of coma as a treatable medical entity.

“It continues to highlight the challenges of prognostication in acute brain injured patients by showing a higher presence of cognitive function than previously perceived,” she said.

Dr. Sarwal believes that the study’s largest impact is underscoring the need for more research into understanding the degree and quality of cognitive processing in patients with a disorder of consciousness. But it also underlines the need for a “healthy debate” on the cost/benefit analysis of pursuing such research, given the limited number of patients with access to resources. 

“This debate needs to include the caregivers and families outside the traditional realms of stakeholders overseeing the science.” 

Although communication with comatose patients is still “a ways away,” this research is “a step in the right direction,” said Dr. Sarwal. 

The study was funded by the James S. McDonnell Foundation and others. Dr. Schiff and Dr. Sarwal report no relevant financial disclosures.
 

A version of this article first appeared on Medscape.com.

At least 25% of unresponsive patients with a disorder of consciousness show signs of brain activity, an estimate that is higher than previous studies suggest.

“We found that at least 1 in 4 patients who are unresponsive to commands might actually be quite present and highly cognitive,” said study investigator Nicholas D. Schiff, MD, Feil Family Brain & Mind Research Institute and Department of Neurology, Weill Cornell Medicine, Rockefeller University Hospital, New York.

“In other words, if you go to the bedside and carefully examine someone with a severe brain injury and find no evidence of responsiveness, no one has been able to give you an a priori number to say how likely you are to be wrong in thinking this person is actually unaware, not processing language, and not capable of high-level cognitive work. And the answer to that now is at least 1 in 4 times.”

The findings were published online in The New England Journal of Medicine.
 

Clinical Implications? 

Cognitive motor dissociation (CMD) is a condition whereby patients with a severe brain injury who are unresponsive to commands at the bedside show brain activity on functional MRI (fMRI) or electroencephalography (EEG) when presented with selective motor imagery commands, such as “imagine playing tennis,” or “ imagine opening and closing your hand.”

Previous research shows that CMD is present in 10%-20% of people with a disorder of consciousness, a rate similar to that in patients with acute or chronic brain injury.

Understanding that a patient who appears unconscious has signs of cognitive processing could change the way clinicians and family interact with such individuals. Unresponsive patients who are aware may eventually be able to harness emerging communication technologies such as brain-computer interfaces.

In addition, knowing an individual’s CMD status could aid in prognosis. “We know from one study that there’s a four times increased likelihood that patients will be independent in a year in their function if they have cognitive motor dissociation,” said Dr. Schiff.

Unlike most previous studies of CMD, which were conducted at single sites and had relatively small cohorts, this new study included 353 adults with a disorder of consciousness (mean age, 37.9 years; 64% male) at six multinational sites.

Participants were recruited using a variety of methods, including consecutive enrollment of critically ill patients in the intensive care unit and enrollment of those with chronic illness or injury who were in the postacute phase of brain injury.
 

Response to Commands

Study participants were at different stages of recovery from an acute brain injury that had occurred an average of 8 months before the study started.

To determine the presence or absence of an observable response to commands among participants, trained staff used the Coma Recovery Scale–Revised (CRS-R); scores on this instrument range from 0 to 23, and higher scores indicate better neurobehavioral function.

About 40% of individuals were diagnosed with coma or vegetative state, 29% with minimally conscious state–minus, and 22% with minimally conscious state–plus. In all, 10% had emerged from a minimally conscious state.

Researchers assessed response to timed and repeated commands using fMRI or EEG in participants without an observable response to verbal commands, including those with a behavioral diagnosis of coma, vegetative state, or minimally conscious state–minus, and in participants with an observable response to verbal commands.

Of the 353 study participants, 61% underwent at least one fMRI assessment and 74% at least one EEG assessment. Both fMRI and EEG were performed in 35% of participants.

Dr. Schiff explained the two assessment types provide slightly different information, in that they measuring different types of brain signals. He also noted that although “every medical center in the world” has EEG, many do not have fMRI.

The brain imaging assessments captured brain activity within the motor area of the frontal cortex when tasked with motor imagery.

Of the 241 participants deemed to be in a coma or vegetative state or minimally conscious state–minus on the basis of CRS-R score, 60 (25%) had a response to commands on task-based fMRI, task-based EEG, or both.

The percentage of participants with CMD varied across study sites, from 2% to 45%, but Dr. Schiff said the reason for this is unclear. 

The proportion of participants with CMD may have been even higher if all individuals had been assessed with both imaging techniques, he said.
 

Higher Rate of Awareness Than in Previous Research

The investigators noted that the percentage of participants with CMD in their study was up to 10 percentage points higher than in previous studies. This may be due to the multimodal approach that classified participants undergoing assessment with both fMRI and EEG on the basis of responses on either technique, they said. 

The median age was lower among participants with CMD than those without CMD (30.5 years vs 45.3 years).

Compared with participants without CMD, a higher percentage of those with such dissociation had brain trauma as an etiologic factor (65% vs 38%) and a diagnosis of minimally conscious state–minus on the CRS-R (53% vs 38%).

Among people with CMD, 18% were assessed with fMRI only, 22% with EEG only, and 60% with both fMRI and EEG.

Dr. Schiff noted that the use of both fMRI and EEG appears to be more sensitive in detecting brain activity during tasks compared with use of one of these techniques alone.

Of the 112 participants with a diagnosis of minimally conscious state–plus or who had emerged from the minimally conscious state, 38% had a response to commands on task-based fMRI, task-based EEG, or both. Among these participants, 23% were assessed with fMRI only, 19% with EEG only, and 58% with both fMRI and EEG.

Research shows “it’s very clear that people with severe brain injury continue to get better over time,” noted Dr. Schiff. “Every month and week matters, and so it probably is the case that a lot of these patients are picking up the level of recovery, and the later we go out to measure them, the more likely we are to find people who are CMD than not.”

These new results should prompt further study to explore whether detection of CMD can lead to improved outcomes, the investigators noted. “In addition, the standardization, validation, and simplification of task-based fMRI and EEG methods that are used to detect cognitive motor dissociation are needed to prompt widespread clinical integration of these techniques and investigation of the bioethical implications of the findings.”

All study participants with chronic brain injury had survived their initial illness or injury and had access to a research facility with advanced fMRI and EEG capabilities. “This survival bias may reflect greater cognitive reserve and resilience over time among the participants. As such, the results of our study may not be generalizable to the overall population of patients with cognitive motor dissociation,” the investigators wrote.

Another study limitation was that participating sites used heterogeneous strategies to acquire, analyze, and interpret data, which led to differences in the number, type, and ordering of the cognitive tasks assessed on fMRI and EEG.

“These differences, along with variations in recruitment strategies and participant characteristics, may have contributed to the unequal percentage of participants with cognitive motor dissociation observed at each site. Our findings may therefore not be generalizable across all centers,” the researchers wrote. 

Only a few academic medical centers have the specially trained personnel and techniques needed to assess patients for CMD — which, the researchers noted, limits the feasibility of performing these assessments in general practice.
 

Challenging Research

Commenting on the research, Aarti Sarwal, MD, professor of neurology and section chief, Neurocritical Care, Virginia Commonwealth University, Richmond, Virginia, noted that this was a “very challenging” study to perform, given that only a few academic centers are equipped to perform both fMRI and quantitative EEG analysis.

“In general, finding patients this far out, who have access to clinical, radiological, and electrophysiological testing and were provided good care enough to receive these, is a mammoth task in itself.” 

Dr. Sarwal said the study builds on efforts of the Curing Coma campaign , a clinical, scientific, and public health effort of the Neurocritical Care Society to tackle the concept of coma as a treatable medical entity.

“It continues to highlight the challenges of prognostication in acute brain injured patients by showing a higher presence of cognitive function than previously perceived,” she said.

Dr. Sarwal believes that the study’s largest impact is underscoring the need for more research into understanding the degree and quality of cognitive processing in patients with a disorder of consciousness. But it also underlines the need for a “healthy debate” on the cost/benefit analysis of pursuing such research, given the limited number of patients with access to resources. 

“This debate needs to include the caregivers and families outside the traditional realms of stakeholders overseeing the science.” 

Although communication with comatose patients is still “a ways away,” this research is “a step in the right direction,” said Dr. Sarwal. 

The study was funded by the James S. McDonnell Foundation and others. Dr. Schiff and Dr. Sarwal report no relevant financial disclosures.
 

A version of this article first appeared on Medscape.com.

At least 25% of unresponsive patients with a disorder of consciousness show signs of brain activity, an estimate that is higher than previous studies suggest.

“We found that at least 1 in 4 patients who are unresponsive to commands might actually be quite present and highly cognitive,” said study investigator Nicholas D. Schiff, MD, Feil Family Brain & Mind Research Institute and Department of Neurology, Weill Cornell Medicine, Rockefeller University Hospital, New York.

“In other words, if you go to the bedside and carefully examine someone with a severe brain injury and find no evidence of responsiveness, no one has been able to give you an a priori number to say how likely you are to be wrong in thinking this person is actually unaware, not processing language, and not capable of high-level cognitive work. And the answer to that now is at least 1 in 4 times.”

The findings were published online in The New England Journal of Medicine.
 

Clinical Implications? 

Cognitive motor dissociation (CMD) is a condition whereby patients with a severe brain injury who are unresponsive to commands at the bedside show brain activity on functional MRI (fMRI) or electroencephalography (EEG) when presented with selective motor imagery commands, such as “imagine playing tennis,” or “ imagine opening and closing your hand.”

Previous research shows that CMD is present in 10%-20% of people with a disorder of consciousness, a rate similar to that in patients with acute or chronic brain injury.

Understanding that a patient who appears unconscious has signs of cognitive processing could change the way clinicians and family interact with such individuals. Unresponsive patients who are aware may eventually be able to harness emerging communication technologies such as brain-computer interfaces.

In addition, knowing an individual’s CMD status could aid in prognosis. “We know from one study that there’s a four times increased likelihood that patients will be independent in a year in their function if they have cognitive motor dissociation,” said Dr. Schiff.

Unlike most previous studies of CMD, which were conducted at single sites and had relatively small cohorts, this new study included 353 adults with a disorder of consciousness (mean age, 37.9 years; 64% male) at six multinational sites.

Participants were recruited using a variety of methods, including consecutive enrollment of critically ill patients in the intensive care unit and enrollment of those with chronic illness or injury who were in the postacute phase of brain injury.
 

Response to Commands

Study participants were at different stages of recovery from an acute brain injury that had occurred an average of 8 months before the study started.

To determine the presence or absence of an observable response to commands among participants, trained staff used the Coma Recovery Scale–Revised (CRS-R); scores on this instrument range from 0 to 23, and higher scores indicate better neurobehavioral function.

About 40% of individuals were diagnosed with coma or vegetative state, 29% with minimally conscious state–minus, and 22% with minimally conscious state–plus. In all, 10% had emerged from a minimally conscious state.

Researchers assessed response to timed and repeated commands using fMRI or EEG in participants without an observable response to verbal commands, including those with a behavioral diagnosis of coma, vegetative state, or minimally conscious state–minus, and in participants with an observable response to verbal commands.

Of the 353 study participants, 61% underwent at least one fMRI assessment and 74% at least one EEG assessment. Both fMRI and EEG were performed in 35% of participants.

Dr. Schiff explained the two assessment types provide slightly different information, in that they measuring different types of brain signals. He also noted that although “every medical center in the world” has EEG, many do not have fMRI.

The brain imaging assessments captured brain activity within the motor area of the frontal cortex when tasked with motor imagery.

Of the 241 participants deemed to be in a coma or vegetative state or minimally conscious state–minus on the basis of CRS-R score, 60 (25%) had a response to commands on task-based fMRI, task-based EEG, or both.

The percentage of participants with CMD varied across study sites, from 2% to 45%, but Dr. Schiff said the reason for this is unclear. 

The proportion of participants with CMD may have been even higher if all individuals had been assessed with both imaging techniques, he said.
 

Higher Rate of Awareness Than in Previous Research

The investigators noted that the percentage of participants with CMD in their study was up to 10 percentage points higher than in previous studies. This may be due to the multimodal approach that classified participants undergoing assessment with both fMRI and EEG on the basis of responses on either technique, they said. 

The median age was lower among participants with CMD than those without CMD (30.5 years vs 45.3 years).

Compared with participants without CMD, a higher percentage of those with such dissociation had brain trauma as an etiologic factor (65% vs 38%) and a diagnosis of minimally conscious state–minus on the CRS-R (53% vs 38%).

Among people with CMD, 18% were assessed with fMRI only, 22% with EEG only, and 60% with both fMRI and EEG.

Dr. Schiff noted that the use of both fMRI and EEG appears to be more sensitive in detecting brain activity during tasks compared with use of one of these techniques alone.

Of the 112 participants with a diagnosis of minimally conscious state–plus or who had emerged from the minimally conscious state, 38% had a response to commands on task-based fMRI, task-based EEG, or both. Among these participants, 23% were assessed with fMRI only, 19% with EEG only, and 58% with both fMRI and EEG.

Research shows “it’s very clear that people with severe brain injury continue to get better over time,” noted Dr. Schiff. “Every month and week matters, and so it probably is the case that a lot of these patients are picking up the level of recovery, and the later we go out to measure them, the more likely we are to find people who are CMD than not.”

These new results should prompt further study to explore whether detection of CMD can lead to improved outcomes, the investigators noted. “In addition, the standardization, validation, and simplification of task-based fMRI and EEG methods that are used to detect cognitive motor dissociation are needed to prompt widespread clinical integration of these techniques and investigation of the bioethical implications of the findings.”

All study participants with chronic brain injury had survived their initial illness or injury and had access to a research facility with advanced fMRI and EEG capabilities. “This survival bias may reflect greater cognitive reserve and resilience over time among the participants. As such, the results of our study may not be generalizable to the overall population of patients with cognitive motor dissociation,” the investigators wrote.

Another study limitation was that participating sites used heterogeneous strategies to acquire, analyze, and interpret data, which led to differences in the number, type, and ordering of the cognitive tasks assessed on fMRI and EEG.

“These differences, along with variations in recruitment strategies and participant characteristics, may have contributed to the unequal percentage of participants with cognitive motor dissociation observed at each site. Our findings may therefore not be generalizable across all centers,” the researchers wrote. 

Only a few academic medical centers have the specially trained personnel and techniques needed to assess patients for CMD — which, the researchers noted, limits the feasibility of performing these assessments in general practice.
 

Challenging Research

Commenting on the research, Aarti Sarwal, MD, professor of neurology and section chief, Neurocritical Care, Virginia Commonwealth University, Richmond, Virginia, noted that this was a “very challenging” study to perform, given that only a few academic centers are equipped to perform both fMRI and quantitative EEG analysis.

“In general, finding patients this far out, who have access to clinical, radiological, and electrophysiological testing and were provided good care enough to receive these, is a mammoth task in itself.” 

Dr. Sarwal said the study builds on efforts of the Curing Coma campaign , a clinical, scientific, and public health effort of the Neurocritical Care Society to tackle the concept of coma as a treatable medical entity.

“It continues to highlight the challenges of prognostication in acute brain injured patients by showing a higher presence of cognitive function than previously perceived,” she said.

Dr. Sarwal believes that the study’s largest impact is underscoring the need for more research into understanding the degree and quality of cognitive processing in patients with a disorder of consciousness. But it also underlines the need for a “healthy debate” on the cost/benefit analysis of pursuing such research, given the limited number of patients with access to resources. 

“This debate needs to include the caregivers and families outside the traditional realms of stakeholders overseeing the science.” 

Although communication with comatose patients is still “a ways away,” this research is “a step in the right direction,” said Dr. Sarwal. 

The study was funded by the James S. McDonnell Foundation and others. Dr. Schiff and Dr. Sarwal report no relevant financial disclosures.
 

A version of this article first appeared on Medscape.com.

A new report on the preventability of dementia is both exciting and paradigm-shifting. The new study, published in The Lancet by the Lancet Commission on Dementia, estimates that close to 50% of cases of dementia worldwide can be prevented or delayed by improving 14 modifiable risk factors. 

This is paradigm-shifting because dementia is often perceived as an inevitable consequence of the aging process, with a major genetic component. But this study suggests that modifying these risk factors can benefit everyone, irrespective of genetic risk, and that it’s important to have a life-course approach. It’s never too early or too late to start to modify these factors. 

We’ve known for a long time that many chronic diseases are highly preventable and modifiable. Some that come to mind are type 2 diabetes, coronary heart disease, and even certain forms of cancer. Modifiable risk factors include cigarette smoking, diet, physical activity, and maintaining a healthy weight. This study suggests that many of the same risk factors and more are relevant to reducing risk for dementia. 

Let’s go through the risk factors, many of which are behavioral. These risk factors include lifestyle factors such as lack of physical activity, cigarette smoking, excessive alcohol consumption, and obesity. The cardiovascular or vascular-specific risk factors include not only those behavioral factors but also hypertension, high LDL cholesterol, and diabetes. Cognitive engagement–specific risk factors include social isolation, which is a major risk factor for dementia, as well as untreated hearing or vision loss, which can exacerbate social isolation and depression, and low educational attainment, which can be related to less cognitive engagement.

They also mention traumatic brain injury from an accident or contact sports without head protection as a risk factor, and the environmental risk factor of air pollution or poor air quality. 

Two of these risk factors are new since the previous report in 2020: elevated LDL cholesterol and untreated vision loss, both of which are quite treatable. Overall, these findings suggest that a lot can be done to lower dementia risk, but it requires individual behavior modifications as well as a comprehensive approach with involvement of the healthcare system for improved screening, access, and public policy to reduce air pollution.

Some of these risk factors are more relevant to women, especially the social isolation that is so common later in life in women. In the United States, close to two out of three patients with dementia are women.

So, informing our patients about these risk factors and what can be done in terms of behavior modification, increased screening, and treatment for these conditions can go a long way in helping our patients reduce their risk for dementia.
 

Dr. Manson is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, chief, Division of Preventive Medicine, Brigham and Women’s Hospital, Boston, and past president, North American Menopause Society, 2011-2012. She disclosed receiving study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).

A version of this article appeared on Medscape.com.

A new report on the preventability of dementia is both exciting and paradigm-shifting. The new study, published in The Lancet by the Lancet Commission on Dementia, estimates that close to 50% of cases of dementia worldwide can be prevented or delayed by improving 14 modifiable risk factors. 

This is paradigm-shifting because dementia is often perceived as an inevitable consequence of the aging process, with a major genetic component. But this study suggests that modifying these risk factors can benefit everyone, irrespective of genetic risk, and that it’s important to have a life-course approach. It’s never too early or too late to start to modify these factors. 

We’ve known for a long time that many chronic diseases are highly preventable and modifiable. Some that come to mind are type 2 diabetes, coronary heart disease, and even certain forms of cancer. Modifiable risk factors include cigarette smoking, diet, physical activity, and maintaining a healthy weight. This study suggests that many of the same risk factors and more are relevant to reducing risk for dementia. 

Let’s go through the risk factors, many of which are behavioral. These risk factors include lifestyle factors such as lack of physical activity, cigarette smoking, excessive alcohol consumption, and obesity. The cardiovascular or vascular-specific risk factors include not only those behavioral factors but also hypertension, high LDL cholesterol, and diabetes. Cognitive engagement–specific risk factors include social isolation, which is a major risk factor for dementia, as well as untreated hearing or vision loss, which can exacerbate social isolation and depression, and low educational attainment, which can be related to less cognitive engagement.

They also mention traumatic brain injury from an accident or contact sports without head protection as a risk factor, and the environmental risk factor of air pollution or poor air quality. 

Two of these risk factors are new since the previous report in 2020: elevated LDL cholesterol and untreated vision loss, both of which are quite treatable. Overall, these findings suggest that a lot can be done to lower dementia risk, but it requires individual behavior modifications as well as a comprehensive approach with involvement of the healthcare system for improved screening, access, and public policy to reduce air pollution.

Some of these risk factors are more relevant to women, especially the social isolation that is so common later in life in women. In the United States, close to two out of three patients with dementia are women.

So, informing our patients about these risk factors and what can be done in terms of behavior modification, increased screening, and treatment for these conditions can go a long way in helping our patients reduce their risk for dementia.
 

Dr. Manson is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, chief, Division of Preventive Medicine, Brigham and Women’s Hospital, Boston, and past president, North American Menopause Society, 2011-2012. She disclosed receiving study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).

A version of this article appeared on Medscape.com.

A new report on the preventability of dementia is both exciting and paradigm-shifting. The new study, published in The Lancet by the Lancet Commission on Dementia, estimates that close to 50% of cases of dementia worldwide can be prevented or delayed by improving 14 modifiable risk factors. 

This is paradigm-shifting because dementia is often perceived as an inevitable consequence of the aging process, with a major genetic component. But this study suggests that modifying these risk factors can benefit everyone, irrespective of genetic risk, and that it’s important to have a life-course approach. It’s never too early or too late to start to modify these factors. 

We’ve known for a long time that many chronic diseases are highly preventable and modifiable. Some that come to mind are type 2 diabetes, coronary heart disease, and even certain forms of cancer. Modifiable risk factors include cigarette smoking, diet, physical activity, and maintaining a healthy weight. This study suggests that many of the same risk factors and more are relevant to reducing risk for dementia. 

Let’s go through the risk factors, many of which are behavioral. These risk factors include lifestyle factors such as lack of physical activity, cigarette smoking, excessive alcohol consumption, and obesity. The cardiovascular or vascular-specific risk factors include not only those behavioral factors but also hypertension, high LDL cholesterol, and diabetes. Cognitive engagement–specific risk factors include social isolation, which is a major risk factor for dementia, as well as untreated hearing or vision loss, which can exacerbate social isolation and depression, and low educational attainment, which can be related to less cognitive engagement.

They also mention traumatic brain injury from an accident or contact sports without head protection as a risk factor, and the environmental risk factor of air pollution or poor air quality. 

Two of these risk factors are new since the previous report in 2020: elevated LDL cholesterol and untreated vision loss, both of which are quite treatable. Overall, these findings suggest that a lot can be done to lower dementia risk, but it requires individual behavior modifications as well as a comprehensive approach with involvement of the healthcare system for improved screening, access, and public policy to reduce air pollution.

Some of these risk factors are more relevant to women, especially the social isolation that is so common later in life in women. In the United States, close to two out of three patients with dementia are women.

So, informing our patients about these risk factors and what can be done in terms of behavior modification, increased screening, and treatment for these conditions can go a long way in helping our patients reduce their risk for dementia.
 

Dr. Manson is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, chief, Division of Preventive Medicine, Brigham and Women’s Hospital, Boston, and past president, North American Menopause Society, 2011-2012. She disclosed receiving study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).

A version of this article appeared on Medscape.com.

Once again, America is deeply divided before a national election, with people on each side convinced of the horrors that will be visited upon us if the other side wins. 

’Tis the season — and regrettably, not to be jolly but to be worried.

As a neuroscientist, I am especially aware of the deleterious mental and physical impact of chronic worry on our citizenry. That’s because worry is not “all in your head.” Chronic mild stress drives a panoply of negative changes in your body and brain that add to your risk for physical and neurologic troubles. We modern humans live in a world of worry which appears to be progressively growing.
 

Flight or Fight

Worry stems from the brain’s rather remarkable ability to foresee and reflexively respond to threat. Our “fight or flight” brain machinery probably arose in our vertebrate ancestors more than 300 million years ago. The fact that we have machinery akin to that possessed by lizards or tigers or shrews is testimony to its crucial contribution to our species’ survival.

As the phrase “fight or flight” suggests, a brain that senses trouble immediately biases certain body and brain functions. As it shifts into a higher-alert mode, it increases the energy supplies in our blood and supports other changes that facilitate faster and stronger reactions, while it shuts down less essential processes which do not contribute to hiding, fighting, or running like hell.

This hyperreactive response is initiated in the amygdala in the anterior brain, which identifies “what’s happening” as immediately or potentially threatening. The now-activated amygdala generates a response in the hypothalamus that provokes an immediate increase of adrenaline and cortisol in the body, and cortisol and noradrenaline in the brain. Both sharply speed up our physical and neurologic reactivity. In the brain, that is achieved by increasing the level of excitability of neurons across the forebrain. Depending on the perceived level of threat, an excitable brain will be just a little or a lot more “on alert,” just a little or a lot faster to respond, and just a little or a lot better at remembering the specific “warning” events that trigger this lizard-brain response. 

Alas, this machinery was designed to be engaged every so often when a potentially dangerous surprise arises in life. When the worry and stress are persistent, the brain experiences a kind of neurologic “burn-out” of its fight versus flight machinery.
 

Dangers of Nonstop Anxiety and Stress

A consistently stressed-out brain turns down its production and release of noradrenaline, and the brain becomes less attentive, less engaged. This sets the brain on the path to an anxiety (and then a depressive) disorder, and, in the longer term, to cognitive losses in memory and executive control systems, and to emotional distortions that can lead to substance abuse or other addictions.

Our political distress is but one source of persistent worry and stress. Worry is a modern plague. The head counts of individuals seeking psychiatric or psychological health are at an all-time high in the United States. Near-universal low-level stressors, such as 2 years of COVID, insecurities about the changing demands of our professional and private lives, and a deeply divided body politic are unequivocally affecting American brain health.

The brain also collaborates in our body’s response to stress. Its regulation of hormonal responses and its autonomic nervous system’s mediated responses contribute to elevated blood sugar levels, to craving high-sugar foods, to elevated blood pressure, and to weaker immune responses. This all contributes to higher risks for cardiovascular and other dietary- and immune system–related disease. And ultimately, to shorter lifespans.
 

Strategies to Address Neurologic Changes Arising From Chronic Stress

There are many things you can try to bring your worry back to a manageable (and even productive) level.

• Engage in a “reset” strategy several times a day to bring your amygdala and locus coeruleus back under control. It takes a minute (or five) of calm, positive meditation to take your brain to a happy, optimistic place. Or use a mindfulness exercise to quiet down that overactive amygdala.
• Talk to people. Keeping your worries to yourself can compound them. Hashing through your concerns with a family member, friend, professional coach, or therapist can help put them in perspective and may allow you to come up with strategies to identify and neurologically respond to your sources of stress.
• Exercise, both physically and mentally. Do what works for you, whether it’s a run, a long walk, pumping iron, playing racquetball — anything that promotes physical release. Exercise your brain too. Engage in a project or activity that is mentally demanding. Personally, I like to garden and do online brain exercises. There’s nothing quite like yanking out weeds or hitting a new personal best at a cognitive exercise for me to notch a sense of accomplishment to counterbalance the unresolved issues driving my worry.
• Accept the uncertainty. Life is full of uncertainty. To paraphrase from Yale theologian Reinhold Niebuhr’s “Serenity Prayer”: Have the serenity to accept what you cannot help, the courage to change what you can, and the wisdom to recognize one from the other.

And, please, be assured that you’ll make it through this election season.

Dr. Merzenich, professor emeritus, Department of Neuroscience, University of California San Francisco, disclosed ties with Posit Science. He is often credited with discovering lifelong plasticity, with being the first to harness plasticity for human benefit (in his co-invention of the cochlear implant), and for pioneering the field of plasticity-based computerized brain exercise. He is a Kavli Laureate in Neuroscience, and he has been honored by each of the US National Academies of Sciences, Engineering, and Medicine. He may be most widely known for a series of specials on the brain on public television. His current focus is  BrainHQ, a brain exercise app.

A version of this article appeared on Medscape.com.

Once again, America is deeply divided before a national election, with people on each side convinced of the horrors that will be visited upon us if the other side wins. 

’Tis the season — and regrettably, not to be jolly but to be worried.

As a neuroscientist, I am especially aware of the deleterious mental and physical impact of chronic worry on our citizenry. That’s because worry is not “all in your head.” Chronic mild stress drives a panoply of negative changes in your body and brain that add to your risk for physical and neurologic troubles. We modern humans live in a world of worry which appears to be progressively growing.
 

Flight or Fight

Worry stems from the brain’s rather remarkable ability to foresee and reflexively respond to threat. Our “fight or flight” brain machinery probably arose in our vertebrate ancestors more than 300 million years ago. The fact that we have machinery akin to that possessed by lizards or tigers or shrews is testimony to its crucial contribution to our species’ survival.

As the phrase “fight or flight” suggests, a brain that senses trouble immediately biases certain body and brain functions. As it shifts into a higher-alert mode, it increases the energy supplies in our blood and supports other changes that facilitate faster and stronger reactions, while it shuts down less essential processes which do not contribute to hiding, fighting, or running like hell.

This hyperreactive response is initiated in the amygdala in the anterior brain, which identifies “what’s happening” as immediately or potentially threatening. The now-activated amygdala generates a response in the hypothalamus that provokes an immediate increase of adrenaline and cortisol in the body, and cortisol and noradrenaline in the brain. Both sharply speed up our physical and neurologic reactivity. In the brain, that is achieved by increasing the level of excitability of neurons across the forebrain. Depending on the perceived level of threat, an excitable brain will be just a little or a lot more “on alert,” just a little or a lot faster to respond, and just a little or a lot better at remembering the specific “warning” events that trigger this lizard-brain response. 

Alas, this machinery was designed to be engaged every so often when a potentially dangerous surprise arises in life. When the worry and stress are persistent, the brain experiences a kind of neurologic “burn-out” of its fight versus flight machinery.
 

Dangers of Nonstop Anxiety and Stress

A consistently stressed-out brain turns down its production and release of noradrenaline, and the brain becomes less attentive, less engaged. This sets the brain on the path to an anxiety (and then a depressive) disorder, and, in the longer term, to cognitive losses in memory and executive control systems, and to emotional distortions that can lead to substance abuse or other addictions.

Our political distress is but one source of persistent worry and stress. Worry is a modern plague. The head counts of individuals seeking psychiatric or psychological health are at an all-time high in the United States. Near-universal low-level stressors, such as 2 years of COVID, insecurities about the changing demands of our professional and private lives, and a deeply divided body politic are unequivocally affecting American brain health.

The brain also collaborates in our body’s response to stress. Its regulation of hormonal responses and its autonomic nervous system’s mediated responses contribute to elevated blood sugar levels, to craving high-sugar foods, to elevated blood pressure, and to weaker immune responses. This all contributes to higher risks for cardiovascular and other dietary- and immune system–related disease. And ultimately, to shorter lifespans.
 

Strategies to Address Neurologic Changes Arising From Chronic Stress

There are many things you can try to bring your worry back to a manageable (and even productive) level.

• Engage in a “reset” strategy several times a day to bring your amygdala and locus coeruleus back under control. It takes a minute (or five) of calm, positive meditation to take your brain to a happy, optimistic place. Or use a mindfulness exercise to quiet down that overactive amygdala.
• Talk to people. Keeping your worries to yourself can compound them. Hashing through your concerns with a family member, friend, professional coach, or therapist can help put them in perspective and may allow you to come up with strategies to identify and neurologically respond to your sources of stress.
• Exercise, both physically and mentally. Do what works for you, whether it’s a run, a long walk, pumping iron, playing racquetball — anything that promotes physical release. Exercise your brain too. Engage in a project or activity that is mentally demanding. Personally, I like to garden and do online brain exercises. There’s nothing quite like yanking out weeds or hitting a new personal best at a cognitive exercise for me to notch a sense of accomplishment to counterbalance the unresolved issues driving my worry.
• Accept the uncertainty. Life is full of uncertainty. To paraphrase from Yale theologian Reinhold Niebuhr’s “Serenity Prayer”: Have the serenity to accept what you cannot help, the courage to change what you can, and the wisdom to recognize one from the other.

And, please, be assured that you’ll make it through this election season.

Dr. Merzenich, professor emeritus, Department of Neuroscience, University of California San Francisco, disclosed ties with Posit Science. He is often credited with discovering lifelong plasticity, with being the first to harness plasticity for human benefit (in his co-invention of the cochlear implant), and for pioneering the field of plasticity-based computerized brain exercise. He is a Kavli Laureate in Neuroscience, and he has been honored by each of the US National Academies of Sciences, Engineering, and Medicine. He may be most widely known for a series of specials on the brain on public television. His current focus is  BrainHQ, a brain exercise app.

A version of this article appeared on Medscape.com.

Once again, America is deeply divided before a national election, with people on each side convinced of the horrors that will be visited upon us if the other side wins. 

’Tis the season — and regrettably, not to be jolly but to be worried.

As a neuroscientist, I am especially aware of the deleterious mental and physical impact of chronic worry on our citizenry. That’s because worry is not “all in your head.” Chronic mild stress drives a panoply of negative changes in your body and brain that add to your risk for physical and neurologic troubles. We modern humans live in a world of worry which appears to be progressively growing.
 

Flight or Fight

Worry stems from the brain’s rather remarkable ability to foresee and reflexively respond to threat. Our “fight or flight” brain machinery probably arose in our vertebrate ancestors more than 300 million years ago. The fact that we have machinery akin to that possessed by lizards or tigers or shrews is testimony to its crucial contribution to our species’ survival.

As the phrase “fight or flight” suggests, a brain that senses trouble immediately biases certain body and brain functions. As it shifts into a higher-alert mode, it increases the energy supplies in our blood and supports other changes that facilitate faster and stronger reactions, while it shuts down less essential processes which do not contribute to hiding, fighting, or running like hell.

This hyperreactive response is initiated in the amygdala in the anterior brain, which identifies “what’s happening” as immediately or potentially threatening. The now-activated amygdala generates a response in the hypothalamus that provokes an immediate increase of adrenaline and cortisol in the body, and cortisol and noradrenaline in the brain. Both sharply speed up our physical and neurologic reactivity. In the brain, that is achieved by increasing the level of excitability of neurons across the forebrain. Depending on the perceived level of threat, an excitable brain will be just a little or a lot more “on alert,” just a little or a lot faster to respond, and just a little or a lot better at remembering the specific “warning” events that trigger this lizard-brain response. 

Alas, this machinery was designed to be engaged every so often when a potentially dangerous surprise arises in life. When the worry and stress are persistent, the brain experiences a kind of neurologic “burn-out” of its fight versus flight machinery.
 

Dangers of Nonstop Anxiety and Stress

A consistently stressed-out brain turns down its production and release of noradrenaline, and the brain becomes less attentive, less engaged. This sets the brain on the path to an anxiety (and then a depressive) disorder, and, in the longer term, to cognitive losses in memory and executive control systems, and to emotional distortions that can lead to substance abuse or other addictions.

Our political distress is but one source of persistent worry and stress. Worry is a modern plague. The head counts of individuals seeking psychiatric or psychological health are at an all-time high in the United States. Near-universal low-level stressors, such as 2 years of COVID, insecurities about the changing demands of our professional and private lives, and a deeply divided body politic are unequivocally affecting American brain health.

The brain also collaborates in our body’s response to stress. Its regulation of hormonal responses and its autonomic nervous system’s mediated responses contribute to elevated blood sugar levels, to craving high-sugar foods, to elevated blood pressure, and to weaker immune responses. This all contributes to higher risks for cardiovascular and other dietary- and immune system–related disease. And ultimately, to shorter lifespans.
 

Strategies to Address Neurologic Changes Arising From Chronic Stress

There are many things you can try to bring your worry back to a manageable (and even productive) level.

• Engage in a “reset” strategy several times a day to bring your amygdala and locus coeruleus back under control. It takes a minute (or five) of calm, positive meditation to take your brain to a happy, optimistic place. Or use a mindfulness exercise to quiet down that overactive amygdala.
• Talk to people. Keeping your worries to yourself can compound them. Hashing through your concerns with a family member, friend, professional coach, or therapist can help put them in perspective and may allow you to come up with strategies to identify and neurologically respond to your sources of stress.
• Exercise, both physically and mentally. Do what works for you, whether it’s a run, a long walk, pumping iron, playing racquetball — anything that promotes physical release. Exercise your brain too. Engage in a project or activity that is mentally demanding. Personally, I like to garden and do online brain exercises. There’s nothing quite like yanking out weeds or hitting a new personal best at a cognitive exercise for me to notch a sense of accomplishment to counterbalance the unresolved issues driving my worry.
• Accept the uncertainty. Life is full of uncertainty. To paraphrase from Yale theologian Reinhold Niebuhr’s “Serenity Prayer”: Have the serenity to accept what you cannot help, the courage to change what you can, and the wisdom to recognize one from the other.

And, please, be assured that you’ll make it through this election season.

Dr. Merzenich, professor emeritus, Department of Neuroscience, University of California San Francisco, disclosed ties with Posit Science. He is often credited with discovering lifelong plasticity, with being the first to harness plasticity for human benefit (in his co-invention of the cochlear implant), and for pioneering the field of plasticity-based computerized brain exercise. He is a Kavli Laureate in Neuroscience, and he has been honored by each of the US National Academies of Sciences, Engineering, and Medicine. He may be most widely known for a series of specials on the brain on public television. His current focus is  BrainHQ, a brain exercise app.

A version of this article appeared on Medscape.com.

TOPLINE:

Both chronic and new-onset anxiety are linked to a threefold increased risk for dementia onset in later life, new research shows.

METHODOLOGY:

• A total of 2132 participants aged 55-85 years (mean age, 76 years) were recruited from the Hunter Community Study. Of these, 53% were women.
• Participants were assessed over three different waves, 5 years apart. Demographic and health-related data were captured at wave 1.
• Researchers used the Kessler Psychological Distress Scale (K10) to measure anxiety at two points: Baseline (wave 1) and first follow-up (wave 2), with a 5-year interval between them. Anxiety was classified as chronic if present during both waves, resolved if only present at wave 1, and new if only appearing at wave 2.
• The primary outcome, incident all-cause dementia, during the follow-up period (maximum 13 years after baseline) was identified using the International Classification of Disease-10 codes.

TAKEAWAY:

• Out of 2132 cognitively healthy participants, 64 developed dementia, with an average time to diagnosis of 10 years. Chronic anxiety was linked to a 2.8-fold increased risk for dementia, while new-onset anxiety was associated with a 3.2-fold increased risk (P = .01).
• Participants younger than 70 years with chronic anxiety had a 4.6-fold increased risk for dementia (P = .03), and those with new-onset anxiety had a 7.2 times higher risk for dementia (P = .004).
• There was no significant risk for dementia in participants with anxiety that had resolved.
• Investigators speculated that individuals with anxiety were more likely to engage in unhealthy lifestyle behaviors, such as poor diet and smoking, which can lead to cardiovascular disease — a condition strongly associated with dementia.

IN PRACTICE: 

“This prospective cohort study used causal inference methods to explore the role of anxiety in promoting the development of dementia,” lead author Kay Khaing, MMed, The University of Newcastle, Australia, wrote in a press release. “The findings suggest that anxiety may be a new risk factor to target in the prevention of dementia and also indicate that treating anxiety may reduce this risk.”

SOURCE: 

Kay Khaing, MMed, of The University of Newcastle, Australia, led the study, which was published online in the Journal of the American Geriatrics Society.

LIMITATIONS: 

Anxiety was measured using K10, which assessed symptoms experienced in the most recent 4 weeks, raising concerns about its accuracy over the entire observation period. The authors acknowledged that despite using a combination of the total K10 score and the anxiety subscale, the overlap of anxiety and depression might not be fully disentangled, leading to residual confounding by depression. Additionally, 33% of participants were lost to follow-up, and those lost had higher anxiety rates at baseline, potentially leading to missing cases of dementia and affecting the effect estimate.

DISCLOSURES: 

This study did not report any funding or conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

A version of this article appeared on Medscape.com.

TOPLINE:

Both chronic and new-onset anxiety are linked to a threefold increased risk for dementia onset in later life, new research shows.

METHODOLOGY:

• A total of 2132 participants aged 55-85 years (mean age, 76 years) were recruited from the Hunter Community Study. Of these, 53% were women.
• Participants were assessed over three different waves, 5 years apart. Demographic and health-related data were captured at wave 1.
• Researchers used the Kessler Psychological Distress Scale (K10) to measure anxiety at two points: Baseline (wave 1) and first follow-up (wave 2), with a 5-year interval between them. Anxiety was classified as chronic if present during both waves, resolved if only present at wave 1, and new if only appearing at wave 2.
• The primary outcome, incident all-cause dementia, during the follow-up period (maximum 13 years after baseline) was identified using the International Classification of Disease-10 codes.

TAKEAWAY:

• Out of 2132 cognitively healthy participants, 64 developed dementia, with an average time to diagnosis of 10 years. Chronic anxiety was linked to a 2.8-fold increased risk for dementia, while new-onset anxiety was associated with a 3.2-fold increased risk (P = .01).
• Participants younger than 70 years with chronic anxiety had a 4.6-fold increased risk for dementia (P = .03), and those with new-onset anxiety had a 7.2 times higher risk for dementia (P = .004).
• There was no significant risk for dementia in participants with anxiety that had resolved.
• Investigators speculated that individuals with anxiety were more likely to engage in unhealthy lifestyle behaviors, such as poor diet and smoking, which can lead to cardiovascular disease — a condition strongly associated with dementia.

IN PRACTICE: 

“This prospective cohort study used causal inference methods to explore the role of anxiety in promoting the development of dementia,” lead author Kay Khaing, MMed, The University of Newcastle, Australia, wrote in a press release. “The findings suggest that anxiety may be a new risk factor to target in the prevention of dementia and also indicate that treating anxiety may reduce this risk.”

SOURCE: 

Kay Khaing, MMed, of The University of Newcastle, Australia, led the study, which was published online in the Journal of the American Geriatrics Society.

LIMITATIONS: 

Anxiety was measured using K10, which assessed symptoms experienced in the most recent 4 weeks, raising concerns about its accuracy over the entire observation period. The authors acknowledged that despite using a combination of the total K10 score and the anxiety subscale, the overlap of anxiety and depression might not be fully disentangled, leading to residual confounding by depression. Additionally, 33% of participants were lost to follow-up, and those lost had higher anxiety rates at baseline, potentially leading to missing cases of dementia and affecting the effect estimate.

DISCLOSURES: 

This study did not report any funding or conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

A version of this article appeared on Medscape.com.

TOPLINE:

Both chronic and new-onset anxiety are linked to a threefold increased risk for dementia onset in later life, new research shows.

METHODOLOGY:

• A total of 2132 participants aged 55-85 years (mean age, 76 years) were recruited from the Hunter Community Study. Of these, 53% were women.
• Participants were assessed over three different waves, 5 years apart. Demographic and health-related data were captured at wave 1.
• Researchers used the Kessler Psychological Distress Scale (K10) to measure anxiety at two points: Baseline (wave 1) and first follow-up (wave 2), with a 5-year interval between them. Anxiety was classified as chronic if present during both waves, resolved if only present at wave 1, and new if only appearing at wave 2.
• The primary outcome, incident all-cause dementia, during the follow-up period (maximum 13 years after baseline) was identified using the International Classification of Disease-10 codes.

TAKEAWAY:

• Out of 2132 cognitively healthy participants, 64 developed dementia, with an average time to diagnosis of 10 years. Chronic anxiety was linked to a 2.8-fold increased risk for dementia, while new-onset anxiety was associated with a 3.2-fold increased risk (P = .01).
• Participants younger than 70 years with chronic anxiety had a 4.6-fold increased risk for dementia (P = .03), and those with new-onset anxiety had a 7.2 times higher risk for dementia (P = .004).
• There was no significant risk for dementia in participants with anxiety that had resolved.
• Investigators speculated that individuals with anxiety were more likely to engage in unhealthy lifestyle behaviors, such as poor diet and smoking, which can lead to cardiovascular disease — a condition strongly associated with dementia.

IN PRACTICE: 

“This prospective cohort study used causal inference methods to explore the role of anxiety in promoting the development of dementia,” lead author Kay Khaing, MMed, The University of Newcastle, Australia, wrote in a press release. “The findings suggest that anxiety may be a new risk factor to target in the prevention of dementia and also indicate that treating anxiety may reduce this risk.”

SOURCE: 

Kay Khaing, MMed, of The University of Newcastle, Australia, led the study, which was published online in the Journal of the American Geriatrics Society.

LIMITATIONS: 

Anxiety was measured using K10, which assessed symptoms experienced in the most recent 4 weeks, raising concerns about its accuracy over the entire observation period. The authors acknowledged that despite using a combination of the total K10 score and the anxiety subscale, the overlap of anxiety and depression might not be fully disentangled, leading to residual confounding by depression. Additionally, 33% of participants were lost to follow-up, and those lost had higher anxiety rates at baseline, potentially leading to missing cases of dementia and affecting the effect estimate.

DISCLOSURES: 

This study did not report any funding or conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

A version of this article appeared on Medscape.com.

Patients experiencing memory problems often come to neurologist David Jones, MD, for second opinions. They repeat questions and sometimes misplace items. Their primary care clinician has suggested they may have Alzheimer’s disease or something else.

In many cases, Dr. Jones, a neurologist with Mayo Clinic in Rochester, Minnesota, performs a series of investigations and finds the patient instead has a different type of neurodegenerative syndrome, one that progresses slowly, seems limited chiefly to loss of memory, and which tests show affects only the limbic system.

The news of diagnosis can be reassuring to patients.

“Memory problems are not always Alzheimer’s disease,” Dr. Jones said. “It’s important to broaden the differential diagnosis and seek diagnostic clarity and precision for patients who experience problems with brain functioning later in life.”

Dr. Jones and colleagues recently published clinical criteria for what they call limbic-predominant amnestic neurodegenerative syndrome (LANS).

Various underlying etiologies are known to cause degeneration of the limbic system, the most frequent being a buildup of deposits of the TAR DNA-binding protein 43 (TDP-43) protein referred to as limbic-predominant, age-related TDP-43 encephalopathy neuropathological change (LATE-NC). LATE-NC first involves the amygdala, followed by the hippocampus, and then the middle frontal gyrus, and is found in about 40% of autopsied brains in people over age of 85 years.

By contrast, amnestic syndromes originating from neocortical degeneration are largely caused by neuropathological changes from Alzheimer’s disease and often present with non-memory features.
 

Criteria for LANS

Broken down into core, standard, and advanced features

Core clinical features:

The patient must present with a slow, amnestic, predominant neurodegenerative syndrome — an insidious onset with gradual progression over 2 or more years — without another condition that better accounts for the clinical deficits.

Standard supportive features:

1. Older age at evaluation.

• Most patients are at least the age of 75 years. Older age increases the likelihood that the amnestic syndrome is caused by degeneration of the limbic system.

2. Mild clinical syndrome.

• A diagnosis of mild cognitive impairment or mild amnestic dementia (ie, a score of ≤ 4 on the Clinical Dementia Rating Sum of Boxes [CDR-SB]) at the first visit.

3. Hippocampal atrophy out of proportion to syndrome severity.

• Hippocampal volume was smaller than expected on MRI, compared with the CDR-SB score.

4. Mildly impaired semantic memory.

Advanced supportive features:

1.Limbic hypometabolism and absence of neocortical degenerative pattern on fludeoxyglucose-18-PET imaging.

2. Low likelihood of significant neocortical tau pathology.


Dr. Jones and colleagues also classified a degree of certainty for LANS to use when making a diagnosis. Those with the highest likelihood meet all core, standard, and advanced features.

Patients with a high likelihood of having LANS meet core features, at least three standard features and one advanced feature; or meet core features, at least two standard features as well as two advanced features. Those with a moderate likelihood meet core features and at least three standard features or meet core features and at least two standard features and one advanced feature. Those with a low likelihood of LANS meet core features and two or fewer standard features.

To develop these criteria, the group screened 218 autopsied patients participating in databases for the Mayo Clinic Study of Aging and the multicenter Alzheimer’s Disease Neuroimaging Initiative. They conducted neuropathological assessments, reviewed MRI and PET scans of the brains, and studied fluid biomarkers from samples of cerebrospinal fluid.

In LANS, the neocortex exhibits normal function, Dr. Jones said. High-level language functions, visual spatial functions, and executive function are preserved, and the disease stays mild for many years. LANS is highly associated with LATE, for which no biomarkers are yet available.

The National Institute on Aging in May 2023 held a workshop on LATE, and a consensus group was formed to publish criteria to help with the diagnosis. Many LANS criteria likely will be in that publication as well, Dr. Jones said.

Several steps lay ahead to improve the definition of LANS, the authors wrote, including conducting prospective studies and developing clinical tools that are sensitive and specific to its cognitive features. The development of in vivo diagnostic markers of TDP-43 pathology is needed to embed LANS into a disease state driven by LATE-NC, according to Dr. Jones’ group. Because LANS is newly defined, clinical trials are needed to determine the best treatments.
 

Heterogeneous Dementia

“We are increasingly recognizing that the syndrome of dementia in older adults is heterogeneous,” said Sudha Seshadri, MD, DM, a behavioral neurologist and founding director of the Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases at the University of Texas Health Science Center at San Antonio.

LANS “is something that needs to be diagnosed early but also needs to be worked up in a nuanced manner, with assessment of the pattern of cognitive deficits, the pattern of brain shrinkage on MRI, and also how the disease progresses over, say, a year,” said Dr. Seshadri. “We need to have both some primary care physicians and geriatricians who are comfortable doing this kind of nuanced advising and others who may refer patients to behavioral neurologists, geriatricians, or psychiatrists who have that kind of expertise.”

About 10% of people presenting to dementia clinics potentially could fit the LANS definition, Dr. Seshadri said. Dr. Seshadri was not a coauthor of the classification article but sees patients in the clinic who fit this description.

“It may be that as we start more freely giving the diagnosis of a possible LANS, the proportion of people will go up,” Dr. Seshadri said.

Primary care physicians can use a variety of assessments to help diagnose dementias, she said. These include the Montreal Cognitive Assessment (MoCA), which takes about 10 minutes to administer, or an MRI to determine the level of hippocampal atrophy. Blood tests for p-tau 217 and other plasma tests can stratify risk and guide referrals to a neurologist. Clinicians also should look for reversible causes of memory complaints, such as deficiencies in vitamin B12, folate, or the thyroid hormone.

“There aren’t enough behavioral neurologists around to work up every single person who has memory problems,” Dr. Seshadri said. “We really need to partner on educating and learning from our primary care partners as to what challenges they face, advocating for them to be able to address that, and then sharing what we know, because what we know is an evolving thing.”

Other tools primary care clinicians can use in the initial evaluation of dementia include the General Practitioner Assessment of Cognition and the Mini-Cog, as part of annual Medicare wellness visits or in response to patient or caregiver concerns about memory, said Allison Kaplan, MD, a family physician at Desert Grove Family Medical in Gilbert, Arizona, who coauthored a point-of-care guide for the American Academy of Family Physicians. Each of these tests takes just 3-4 minutes to administer.

If a patient has a positive result on the Mini-Cog or similar test, they should return for further dementia evaluation using the MoCA, Mini-Mental State Examination, or Saint Louis University Mental Status examination, she said. Physicians also can order brain imaging and lab work, as Dr. Seshadri noted. Dementias often accompany some type of cardiovascular disease, which should be managed.

Even if a patient or family member doesn’t express concern about memory, physicians can look for certain signs during medical visits.

“Patients will keep asking the same question, or you notice they’re having difficulty taking care of themselves, especially independent activities of daily living, which could clue you in to a dementia diagnosis,” she said.

Dr. Jones ,Dr. Seshadri, and Dr. Kaplan disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Patients experiencing memory problems often come to neurologist David Jones, MD, for second opinions. They repeat questions and sometimes misplace items. Their primary care clinician has suggested they may have Alzheimer’s disease or something else.

In many cases, Dr. Jones, a neurologist with Mayo Clinic in Rochester, Minnesota, performs a series of investigations and finds the patient instead has a different type of neurodegenerative syndrome, one that progresses slowly, seems limited chiefly to loss of memory, and which tests show affects only the limbic system.

The news of diagnosis can be reassuring to patients.

“Memory problems are not always Alzheimer’s disease,” Dr. Jones said. “It’s important to broaden the differential diagnosis and seek diagnostic clarity and precision for patients who experience problems with brain functioning later in life.”

Dr. Jones and colleagues recently published clinical criteria for what they call limbic-predominant amnestic neurodegenerative syndrome (LANS).

Various underlying etiologies are known to cause degeneration of the limbic system, the most frequent being a buildup of deposits of the TAR DNA-binding protein 43 (TDP-43) protein referred to as limbic-predominant, age-related TDP-43 encephalopathy neuropathological change (LATE-NC). LATE-NC first involves the amygdala, followed by the hippocampus, and then the middle frontal gyrus, and is found in about 40% of autopsied brains in people over age of 85 years.

By contrast, amnestic syndromes originating from neocortical degeneration are largely caused by neuropathological changes from Alzheimer’s disease and often present with non-memory features.
 

Criteria for LANS

Broken down into core, standard, and advanced features

Core clinical features:

The patient must present with a slow, amnestic, predominant neurodegenerative syndrome — an insidious onset with gradual progression over 2 or more years — without another condition that better accounts for the clinical deficits.

Standard supportive features:

1. Older age at evaluation.

• Most patients are at least the age of 75 years. Older age increases the likelihood that the amnestic syndrome is caused by degeneration of the limbic system.

2. Mild clinical syndrome.

• A diagnosis of mild cognitive impairment or mild amnestic dementia (ie, a score of ≤ 4 on the Clinical Dementia Rating Sum of Boxes [CDR-SB]) at the first visit.

3. Hippocampal atrophy out of proportion to syndrome severity.

• Hippocampal volume was smaller than expected on MRI, compared with the CDR-SB score.

4. Mildly impaired semantic memory.

Advanced supportive features:

1.Limbic hypometabolism and absence of neocortical degenerative pattern on fludeoxyglucose-18-PET imaging.

2. Low likelihood of significant neocortical tau pathology.


Dr. Jones and colleagues also classified a degree of certainty for LANS to use when making a diagnosis. Those with the highest likelihood meet all core, standard, and advanced features.

Patients with a high likelihood of having LANS meet core features, at least three standard features and one advanced feature; or meet core features, at least two standard features as well as two advanced features. Those with a moderate likelihood meet core features and at least three standard features or meet core features and at least two standard features and one advanced feature. Those with a low likelihood of LANS meet core features and two or fewer standard features.

To develop these criteria, the group screened 218 autopsied patients participating in databases for the Mayo Clinic Study of Aging and the multicenter Alzheimer’s Disease Neuroimaging Initiative. They conducted neuropathological assessments, reviewed MRI and PET scans of the brains, and studied fluid biomarkers from samples of cerebrospinal fluid.

In LANS, the neocortex exhibits normal function, Dr. Jones said. High-level language functions, visual spatial functions, and executive function are preserved, and the disease stays mild for many years. LANS is highly associated with LATE, for which no biomarkers are yet available.

The National Institute on Aging in May 2023 held a workshop on LATE, and a consensus group was formed to publish criteria to help with the diagnosis. Many LANS criteria likely will be in that publication as well, Dr. Jones said.

Several steps lay ahead to improve the definition of LANS, the authors wrote, including conducting prospective studies and developing clinical tools that are sensitive and specific to its cognitive features. The development of in vivo diagnostic markers of TDP-43 pathology is needed to embed LANS into a disease state driven by LATE-NC, according to Dr. Jones’ group. Because LANS is newly defined, clinical trials are needed to determine the best treatments.
 

Heterogeneous Dementia

“We are increasingly recognizing that the syndrome of dementia in older adults is heterogeneous,” said Sudha Seshadri, MD, DM, a behavioral neurologist and founding director of the Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases at the University of Texas Health Science Center at San Antonio.

LANS “is something that needs to be diagnosed early but also needs to be worked up in a nuanced manner, with assessment of the pattern of cognitive deficits, the pattern of brain shrinkage on MRI, and also how the disease progresses over, say, a year,” said Dr. Seshadri. “We need to have both some primary care physicians and geriatricians who are comfortable doing this kind of nuanced advising and others who may refer patients to behavioral neurologists, geriatricians, or psychiatrists who have that kind of expertise.”

About 10% of people presenting to dementia clinics potentially could fit the LANS definition, Dr. Seshadri said. Dr. Seshadri was not a coauthor of the classification article but sees patients in the clinic who fit this description.

“It may be that as we start more freely giving the diagnosis of a possible LANS, the proportion of people will go up,” Dr. Seshadri said.

Primary care physicians can use a variety of assessments to help diagnose dementias, she said. These include the Montreal Cognitive Assessment (MoCA), which takes about 10 minutes to administer, or an MRI to determine the level of hippocampal atrophy. Blood tests for p-tau 217 and other plasma tests can stratify risk and guide referrals to a neurologist. Clinicians also should look for reversible causes of memory complaints, such as deficiencies in vitamin B12, folate, or the thyroid hormone.

“There aren’t enough behavioral neurologists around to work up every single person who has memory problems,” Dr. Seshadri said. “We really need to partner on educating and learning from our primary care partners as to what challenges they face, advocating for them to be able to address that, and then sharing what we know, because what we know is an evolving thing.”

Other tools primary care clinicians can use in the initial evaluation of dementia include the General Practitioner Assessment of Cognition and the Mini-Cog, as part of annual Medicare wellness visits or in response to patient or caregiver concerns about memory, said Allison Kaplan, MD, a family physician at Desert Grove Family Medical in Gilbert, Arizona, who coauthored a point-of-care guide for the American Academy of Family Physicians. Each of these tests takes just 3-4 minutes to administer.

If a patient has a positive result on the Mini-Cog or similar test, they should return for further dementia evaluation using the MoCA, Mini-Mental State Examination, or Saint Louis University Mental Status examination, she said. Physicians also can order brain imaging and lab work, as Dr. Seshadri noted. Dementias often accompany some type of cardiovascular disease, which should be managed.

Even if a patient or family member doesn’t express concern about memory, physicians can look for certain signs during medical visits.

“Patients will keep asking the same question, or you notice they’re having difficulty taking care of themselves, especially independent activities of daily living, which could clue you in to a dementia diagnosis,” she said.

Dr. Jones ,Dr. Seshadri, and Dr. Kaplan disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Patients experiencing memory problems often come to neurologist David Jones, MD, for second opinions. They repeat questions and sometimes misplace items. Their primary care clinician has suggested they may have Alzheimer’s disease or something else.

In many cases, Dr. Jones, a neurologist with Mayo Clinic in Rochester, Minnesota, performs a series of investigations and finds the patient instead has a different type of neurodegenerative syndrome, one that progresses slowly, seems limited chiefly to loss of memory, and which tests show affects only the limbic system.

The news of diagnosis can be reassuring to patients.

“Memory problems are not always Alzheimer’s disease,” Dr. Jones said. “It’s important to broaden the differential diagnosis and seek diagnostic clarity and precision for patients who experience problems with brain functioning later in life.”

Dr. Jones and colleagues recently published clinical criteria for what they call limbic-predominant amnestic neurodegenerative syndrome (LANS).

Various underlying etiologies are known to cause degeneration of the limbic system, the most frequent being a buildup of deposits of the TAR DNA-binding protein 43 (TDP-43) protein referred to as limbic-predominant, age-related TDP-43 encephalopathy neuropathological change (LATE-NC). LATE-NC first involves the amygdala, followed by the hippocampus, and then the middle frontal gyrus, and is found in about 40% of autopsied brains in people over age of 85 years.

By contrast, amnestic syndromes originating from neocortical degeneration are largely caused by neuropathological changes from Alzheimer’s disease and often present with non-memory features.
 

Criteria for LANS

Broken down into core, standard, and advanced features

Core clinical features:

The patient must present with a slow, amnestic, predominant neurodegenerative syndrome — an insidious onset with gradual progression over 2 or more years — without another condition that better accounts for the clinical deficits.

Standard supportive features:

1. Older age at evaluation.

• Most patients are at least the age of 75 years. Older age increases the likelihood that the amnestic syndrome is caused by degeneration of the limbic system.

2. Mild clinical syndrome.

• A diagnosis of mild cognitive impairment or mild amnestic dementia (ie, a score of ≤ 4 on the Clinical Dementia Rating Sum of Boxes [CDR-SB]) at the first visit.

3. Hippocampal atrophy out of proportion to syndrome severity.

• Hippocampal volume was smaller than expected on MRI, compared with the CDR-SB score.

4. Mildly impaired semantic memory.

Advanced supportive features:

1.Limbic hypometabolism and absence of neocortical degenerative pattern on fludeoxyglucose-18-PET imaging.

2. Low likelihood of significant neocortical tau pathology.


Dr. Jones and colleagues also classified a degree of certainty for LANS to use when making a diagnosis. Those with the highest likelihood meet all core, standard, and advanced features.

Patients with a high likelihood of having LANS meet core features, at least three standard features and one advanced feature; or meet core features, at least two standard features as well as two advanced features. Those with a moderate likelihood meet core features and at least three standard features or meet core features and at least two standard features and one advanced feature. Those with a low likelihood of LANS meet core features and two or fewer standard features.

To develop these criteria, the group screened 218 autopsied patients participating in databases for the Mayo Clinic Study of Aging and the multicenter Alzheimer’s Disease Neuroimaging Initiative. They conducted neuropathological assessments, reviewed MRI and PET scans of the brains, and studied fluid biomarkers from samples of cerebrospinal fluid.

In LANS, the neocortex exhibits normal function, Dr. Jones said. High-level language functions, visual spatial functions, and executive function are preserved, and the disease stays mild for many years. LANS is highly associated with LATE, for which no biomarkers are yet available.

The National Institute on Aging in May 2023 held a workshop on LATE, and a consensus group was formed to publish criteria to help with the diagnosis. Many LANS criteria likely will be in that publication as well, Dr. Jones said.

Several steps lay ahead to improve the definition of LANS, the authors wrote, including conducting prospective studies and developing clinical tools that are sensitive and specific to its cognitive features. The development of in vivo diagnostic markers of TDP-43 pathology is needed to embed LANS into a disease state driven by LATE-NC, according to Dr. Jones’ group. Because LANS is newly defined, clinical trials are needed to determine the best treatments.
 

Heterogeneous Dementia

“We are increasingly recognizing that the syndrome of dementia in older adults is heterogeneous,” said Sudha Seshadri, MD, DM, a behavioral neurologist and founding director of the Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases at the University of Texas Health Science Center at San Antonio.

LANS “is something that needs to be diagnosed early but also needs to be worked up in a nuanced manner, with assessment of the pattern of cognitive deficits, the pattern of brain shrinkage on MRI, and also how the disease progresses over, say, a year,” said Dr. Seshadri. “We need to have both some primary care physicians and geriatricians who are comfortable doing this kind of nuanced advising and others who may refer patients to behavioral neurologists, geriatricians, or psychiatrists who have that kind of expertise.”

About 10% of people presenting to dementia clinics potentially could fit the LANS definition, Dr. Seshadri said. Dr. Seshadri was not a coauthor of the classification article but sees patients in the clinic who fit this description.

“It may be that as we start more freely giving the diagnosis of a possible LANS, the proportion of people will go up,” Dr. Seshadri said.

Primary care physicians can use a variety of assessments to help diagnose dementias, she said. These include the Montreal Cognitive Assessment (MoCA), which takes about 10 minutes to administer, or an MRI to determine the level of hippocampal atrophy. Blood tests for p-tau 217 and other plasma tests can stratify risk and guide referrals to a neurologist. Clinicians also should look for reversible causes of memory complaints, such as deficiencies in vitamin B12, folate, or the thyroid hormone.

“There aren’t enough behavioral neurologists around to work up every single person who has memory problems,” Dr. Seshadri said. “We really need to partner on educating and learning from our primary care partners as to what challenges they face, advocating for them to be able to address that, and then sharing what we know, because what we know is an evolving thing.”

Other tools primary care clinicians can use in the initial evaluation of dementia include the General Practitioner Assessment of Cognition and the Mini-Cog, as part of annual Medicare wellness visits or in response to patient or caregiver concerns about memory, said Allison Kaplan, MD, a family physician at Desert Grove Family Medical in Gilbert, Arizona, who coauthored a point-of-care guide for the American Academy of Family Physicians. Each of these tests takes just 3-4 minutes to administer.

If a patient has a positive result on the Mini-Cog or similar test, they should return for further dementia evaluation using the MoCA, Mini-Mental State Examination, or Saint Louis University Mental Status examination, she said. Physicians also can order brain imaging and lab work, as Dr. Seshadri noted. Dementias often accompany some type of cardiovascular disease, which should be managed.

Even if a patient or family member doesn’t express concern about memory, physicians can look for certain signs during medical visits.

“Patients will keep asking the same question, or you notice they’re having difficulty taking care of themselves, especially independent activities of daily living, which could clue you in to a dementia diagnosis,” she said.

Dr. Jones ,Dr. Seshadri, and Dr. Kaplan disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

A multicomponent nonpharmaceutical intervention improves sleep in people with dementia living at home, early results of a new phase 3 randomized controlled trial (RCT) show.

The benefits of the intervention — called DREAMS-START — were sustained at 8 months and extended to caregivers, the study found.

“We’re pleased with our results. We think that we were able to deliver it successfully and to a high rate of fidelity,” said study investigator Penny Rapaport, PhD, Division of Psychiatry, University College London, England.

The findings were presented at the Alzheimer’s Association International Conference (AAIC) 2024.
 

Sustained, Long-Term Effect

Sleep disturbances are very common in dementia. About 26% of people with all types of dementia will experience sleep disturbances, and that rate is higher in certain dementia subtypes, such as dementia with Lewy bodies, said Dr. Rapaport.

Such disturbances are distressing for people living with dementia as well as for those supporting them, she added. They’re “often the thing that will lead to people transitioning and moving into a care home.”

Dr. Rapaport noted there has not been full RCT evidence that any nonpharmacologic interventions or light-based treatments are effective in improving sleep disturbances.

Medications such as antipsychotics and benzodiazepines aren’t recommended as first-line treatment in people with dementia “because often these can be harmful,” she said.

The study recruited 377 dyads of people living with dementia (mean age, 79.4 years) and their caregivers from 12 national health service sites across England. “We were able to recruit an ethnically diverse sample from a broad socioeconomic background,” said Dr. Rapaport.

Researchers allocated the dyads to the intervention or to a treatment as usual group.

About 92% of participants were included in the intention-to-treat analysis at 8 months, which was the primary time point.

The intervention consists of six 1-hour interactive sessions that are “personalized and tailored to individual goals and needs,” said Dr. Rapaport. It was delivered by supervised, trained graduates, not clinicians.

The sessions focused on components of sleep hygiene (healthy habits, behaviors, and environments); activity and exercise; a tailored sleep routine; strategies to manage distress; natural and artificial light; and relaxation. A whole session was devoted to supporting sleep of caregivers.

The trial included masked outcome assessments, “so the people collecting the data were blinded to the intervention group,” said Dr. Rapaport.

The primary outcome was the Sleep Disorders Inventory (SDI) score. The SDI is a questionnaire about frequency and severity of sleep-disturbed behaviors completed by caregivers; a higher score indicates a worse outcome. The study adjusted for baseline SDI score and study site.

The adjusted mean difference between groups on the SDI was −4.7 points (95% confidence interval [CI], −7.65 to −1.74; P = .002) at 8 months.

The minimal clinically important difference on the SDI is a 4-point change, noted Dr. Rapaport.

The adjusted mean difference on the SDI at 4 months (a secondary outcome) was −4.4 points (95% CI, −7.3 to −1.5; P = .003).

Referring to illustrative graphs, Dr. Rapaport said that SDI scores decreased at both 4 and 8 months. “You can see statistically, there’s a significant difference between groups at both time points,” she said.

“We saw a sustained effect, so not just immediately after the intervention, but afterwards at 8 months.”

As for other secondary outcomes, the study found a significant reduction in neuropsychiatric symptoms among people with dementia at 8 months in the intervention arm relative to the control arm.

In addition, sleep and anxiety significantly improved among caregivers after 8 months. This shows “a picture of things getting better for the person with dementia, and the person who’s caring for them,” said Dr. Rapaport.

She noted the good adherence rate, with almost 83% of people in the intervention arm completing four or more sessions.

Fidelity to the intervention (ie, the extent to which it is implemented as intended) was also high, “so we feel it was delivered well,” said Dr. Rapaport.

Researchers also carried out a health economics analysis and looked at strategies for implementation of the program, but Dr. Rapaport did not discuss those results.
 

Encouraging Findings

Commenting for this news organization, Alex Bahar-Fuchs, PhD, Faculty of Health, School of Psychology, Deakin University, Victoria, Australia, who co-chaired the session featuring the research, said the findings of this “well-powered” RCT are “encouraging,” both for the primary outcome of sleep quality and for some of the secondary outcomes for the care-partner.

“The study adds to the growing evidence behind several nonpharmacological treatment approaches for cognitive and neuropsychiatric symptoms of people with dementia,” he said. 

The results “offer some hope for the treatment of a common disturbance in people with dementia which is associated with poorer outcomes and increased caregiver burden,” he added. 

An important area for further work would be to incorporate more objective measures of sleep quality, said Dr. Bahar-Fuchs.

Because the primary outcome was measured using a self-report questionnaire (the SDI) completed by care-partners, and because the intervention arm could not be blinded, “it remains possible that some detection bias may have affected the study findings,” said Dr. Bahar-Fuchs.

He said he would like to see the research extended to include an active control condition “to be able to better ascertain treatment mechanisms.”

The study was supported by the National Institute of Health and Care Research. Dr. Rapaport and Dr. Bahar-Fuchs reported no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

A multicomponent nonpharmaceutical intervention improves sleep in people with dementia living at home, early results of a new phase 3 randomized controlled trial (RCT) show.

The benefits of the intervention — called DREAMS-START — were sustained at 8 months and extended to caregivers, the study found.

“We’re pleased with our results. We think that we were able to deliver it successfully and to a high rate of fidelity,” said study investigator Penny Rapaport, PhD, Division of Psychiatry, University College London, England.

The findings were presented at the Alzheimer’s Association International Conference (AAIC) 2024.
 

Sustained, Long-Term Effect

Sleep disturbances are very common in dementia. About 26% of people with all types of dementia will experience sleep disturbances, and that rate is higher in certain dementia subtypes, such as dementia with Lewy bodies, said Dr. Rapaport.

Such disturbances are distressing for people living with dementia as well as for those supporting them, she added. They’re “often the thing that will lead to people transitioning and moving into a care home.”

Dr. Rapaport noted there has not been full RCT evidence that any nonpharmacologic interventions or light-based treatments are effective in improving sleep disturbances.

Medications such as antipsychotics and benzodiazepines aren’t recommended as first-line treatment in people with dementia “because often these can be harmful,” she said.

The study recruited 377 dyads of people living with dementia (mean age, 79.4 years) and their caregivers from 12 national health service sites across England. “We were able to recruit an ethnically diverse sample from a broad socioeconomic background,” said Dr. Rapaport.

Researchers allocated the dyads to the intervention or to a treatment as usual group.

About 92% of participants were included in the intention-to-treat analysis at 8 months, which was the primary time point.

The intervention consists of six 1-hour interactive sessions that are “personalized and tailored to individual goals and needs,” said Dr. Rapaport. It was delivered by supervised, trained graduates, not clinicians.

The sessions focused on components of sleep hygiene (healthy habits, behaviors, and environments); activity and exercise; a tailored sleep routine; strategies to manage distress; natural and artificial light; and relaxation. A whole session was devoted to supporting sleep of caregivers.

The trial included masked outcome assessments, “so the people collecting the data were blinded to the intervention group,” said Dr. Rapaport.

The primary outcome was the Sleep Disorders Inventory (SDI) score. The SDI is a questionnaire about frequency and severity of sleep-disturbed behaviors completed by caregivers; a higher score indicates a worse outcome. The study adjusted for baseline SDI score and study site.

The adjusted mean difference between groups on the SDI was −4.7 points (95% confidence interval [CI], −7.65 to −1.74; P = .002) at 8 months.

The minimal clinically important difference on the SDI is a 4-point change, noted Dr. Rapaport.

The adjusted mean difference on the SDI at 4 months (a secondary outcome) was −4.4 points (95% CI, −7.3 to −1.5; P = .003).

Referring to illustrative graphs, Dr. Rapaport said that SDI scores decreased at both 4 and 8 months. “You can see statistically, there’s a significant difference between groups at both time points,” she said.

“We saw a sustained effect, so not just immediately after the intervention, but afterwards at 8 months.”

As for other secondary outcomes, the study found a significant reduction in neuropsychiatric symptoms among people with dementia at 8 months in the intervention arm relative to the control arm.

In addition, sleep and anxiety significantly improved among caregivers after 8 months. This shows “a picture of things getting better for the person with dementia, and the person who’s caring for them,” said Dr. Rapaport.

She noted the good adherence rate, with almost 83% of people in the intervention arm completing four or more sessions.

Fidelity to the intervention (ie, the extent to which it is implemented as intended) was also high, “so we feel it was delivered well,” said Dr. Rapaport.

Researchers also carried out a health economics analysis and looked at strategies for implementation of the program, but Dr. Rapaport did not discuss those results.
 

Encouraging Findings

Commenting for this news organization, Alex Bahar-Fuchs, PhD, Faculty of Health, School of Psychology, Deakin University, Victoria, Australia, who co-chaired the session featuring the research, said the findings of this “well-powered” RCT are “encouraging,” both for the primary outcome of sleep quality and for some of the secondary outcomes for the care-partner.

“The study adds to the growing evidence behind several nonpharmacological treatment approaches for cognitive and neuropsychiatric symptoms of people with dementia,” he said. 

The results “offer some hope for the treatment of a common disturbance in people with dementia which is associated with poorer outcomes and increased caregiver burden,” he added. 

An important area for further work would be to incorporate more objective measures of sleep quality, said Dr. Bahar-Fuchs.

Because the primary outcome was measured using a self-report questionnaire (the SDI) completed by care-partners, and because the intervention arm could not be blinded, “it remains possible that some detection bias may have affected the study findings,” said Dr. Bahar-Fuchs.

He said he would like to see the research extended to include an active control condition “to be able to better ascertain treatment mechanisms.”

The study was supported by the National Institute of Health and Care Research. Dr. Rapaport and Dr. Bahar-Fuchs reported no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

A multicomponent nonpharmaceutical intervention improves sleep in people with dementia living at home, early results of a new phase 3 randomized controlled trial (RCT) show.

The benefits of the intervention — called DREAMS-START — were sustained at 8 months and extended to caregivers, the study found.

“We’re pleased with our results. We think that we were able to deliver it successfully and to a high rate of fidelity,” said study investigator Penny Rapaport, PhD, Division of Psychiatry, University College London, England.

The findings were presented at the Alzheimer’s Association International Conference (AAIC) 2024.
 

Sustained, Long-Term Effect

Sleep disturbances are very common in dementia. About 26% of people with all types of dementia will experience sleep disturbances, and that rate is higher in certain dementia subtypes, such as dementia with Lewy bodies, said Dr. Rapaport.

Such disturbances are distressing for people living with dementia as well as for those supporting them, she added. They’re “often the thing that will lead to people transitioning and moving into a care home.”

Dr. Rapaport noted there has not been full RCT evidence that any nonpharmacologic interventions or light-based treatments are effective in improving sleep disturbances.

Medications such as antipsychotics and benzodiazepines aren’t recommended as first-line treatment in people with dementia “because often these can be harmful,” she said.

The study recruited 377 dyads of people living with dementia (mean age, 79.4 years) and their caregivers from 12 national health service sites across England. “We were able to recruit an ethnically diverse sample from a broad socioeconomic background,” said Dr. Rapaport.

Researchers allocated the dyads to the intervention or to a treatment as usual group.

About 92% of participants were included in the intention-to-treat analysis at 8 months, which was the primary time point.

The intervention consists of six 1-hour interactive sessions that are “personalized and tailored to individual goals and needs,” said Dr. Rapaport. It was delivered by supervised, trained graduates, not clinicians.

The sessions focused on components of sleep hygiene (healthy habits, behaviors, and environments); activity and exercise; a tailored sleep routine; strategies to manage distress; natural and artificial light; and relaxation. A whole session was devoted to supporting sleep of caregivers.

The trial included masked outcome assessments, “so the people collecting the data were blinded to the intervention group,” said Dr. Rapaport.

The primary outcome was the Sleep Disorders Inventory (SDI) score. The SDI is a questionnaire about frequency and severity of sleep-disturbed behaviors completed by caregivers; a higher score indicates a worse outcome. The study adjusted for baseline SDI score and study site.

The adjusted mean difference between groups on the SDI was −4.7 points (95% confidence interval [CI], −7.65 to −1.74; P = .002) at 8 months.

The minimal clinically important difference on the SDI is a 4-point change, noted Dr. Rapaport.

The adjusted mean difference on the SDI at 4 months (a secondary outcome) was −4.4 points (95% CI, −7.3 to −1.5; P = .003).

Referring to illustrative graphs, Dr. Rapaport said that SDI scores decreased at both 4 and 8 months. “You can see statistically, there’s a significant difference between groups at both time points,” she said.

“We saw a sustained effect, so not just immediately after the intervention, but afterwards at 8 months.”

As for other secondary outcomes, the study found a significant reduction in neuropsychiatric symptoms among people with dementia at 8 months in the intervention arm relative to the control arm.

In addition, sleep and anxiety significantly improved among caregivers after 8 months. This shows “a picture of things getting better for the person with dementia, and the person who’s caring for them,” said Dr. Rapaport.

She noted the good adherence rate, with almost 83% of people in the intervention arm completing four or more sessions.

Fidelity to the intervention (ie, the extent to which it is implemented as intended) was also high, “so we feel it was delivered well,” said Dr. Rapaport.

Researchers also carried out a health economics analysis and looked at strategies for implementation of the program, but Dr. Rapaport did not discuss those results.
 

Encouraging Findings

Commenting for this news organization, Alex Bahar-Fuchs, PhD, Faculty of Health, School of Psychology, Deakin University, Victoria, Australia, who co-chaired the session featuring the research, said the findings of this “well-powered” RCT are “encouraging,” both for the primary outcome of sleep quality and for some of the secondary outcomes for the care-partner.

“The study adds to the growing evidence behind several nonpharmacological treatment approaches for cognitive and neuropsychiatric symptoms of people with dementia,” he said. 

The results “offer some hope for the treatment of a common disturbance in people with dementia which is associated with poorer outcomes and increased caregiver burden,” he added. 

An important area for further work would be to incorporate more objective measures of sleep quality, said Dr. Bahar-Fuchs.

Because the primary outcome was measured using a self-report questionnaire (the SDI) completed by care-partners, and because the intervention arm could not be blinded, “it remains possible that some detection bias may have affected the study findings,” said Dr. Bahar-Fuchs.

He said he would like to see the research extended to include an active control condition “to be able to better ascertain treatment mechanisms.”

The study was supported by the National Institute of Health and Care Research. Dr. Rapaport and Dr. Bahar-Fuchs reported no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

PHILADELPHIA – Drinking more than three cups of coffee a day is linked to more rapid cognitive decline over time, results from a large study suggest.

Investigators examined the impact of different amounts of coffee and tea on fluid intelligence — a measure of cognitive functions including abstract reasoning, pattern recognition, and logical thinking.

“It’s the old adage that too much of anything isn’t good. It’s all about balance, so moderate coffee consumption is okay but too much is probably not recommended,” said study investigator Kelsey R. Sewell, PhD, Advent Health Research Institute, Orlando, Florida. 

The findings of the study were presented at the 2024 Alzheimer’s Association International Conference (AAIC).
 

One of the World’s Most Widely Consumed Beverages

Coffee is one of the most widely consumed beverages around the world. The beans contain a range of bioactive compounds, including caffeine, chlorogenic acid, and small amounts of vitamins and minerals.

Consistent evidence from observational and epidemiologic studies indicates that intake of both coffee and tea has beneficial effects on stroke, heart failure, cancers, diabetes, and Parkinson’s disease.  

Several studies also suggest that coffee may reduce the risk for Alzheimer’s disease, said Dr. Sewell. However, there are limited longitudinal data on associations between coffee and tea intake and cognitive decline, particularly in distinct cognitive domains.

Dr. Sewell’s group previously published a study of cognitively unimpaired older adults that found greater coffee consumption was associated with slower cognitive decline and slower accumulation of brain beta-amyloid.

Their current study extends some of the prior findings and investigates the relationship between both coffee and tea intake and cognitive decline over time in a larger sample of older adults.

This new study included 8451 mostly female (60%) and White (97%) cognitively unimpaired adults older than 60 (mean age, 67.8 years) in the UK Biobank, a large-scale research resource containing in-depth, deidentified genetic and health information from half a million UK participants. Study subjects had a mean body mass index (BMI) of 26, and about 26% were apolipoprotein epsilon 4 (APOE e4) gene carriers.

Researchers divided coffee and tea consumption into tertiles: high, moderate, and no consumption.

For daily coffee consumption, 18% reported drinking four or more cups (high consumption), 58% reported drinking one to three cups (moderate consumption), and 25% reported that they never drink coffee. For daily tea consumption, 47% reported drinking four or more cups (high consumption), 38% reported drinking one to three cups (moderate consumption), and 15% reported that they never drink tea.

The study assessed cognitive function at baseline and at least two additional patient visits. 

Researchers used linear mixed models to assess the relationships between coffee and tea intake and cognitive outcomes. The models adjusted for age, sex, Townsend deprivation index (reflecting socioeconomic status), ethnicity, APOE e4 status, and BMI.
 

Steeper Decline 

Compared with high coffee consumption (four or more cups daily), people who never consumed coffee (beta, 0.06; standard error [SE], 0.02; P = .005) and those with moderate consumption (beta, 0.07; SE, 0.02; P = < .001) had slower decline in fluid intelligence after an average of 8.83 years of follow-up.

“We can see that those with high coffee consumption showed the steepest decline in fluid intelligence across the follow up, compared to those with moderate coffee consumption and those never consuming coffee,” said Dr. Sewell, referring to illustrative graphs.

At the same time, “our data suggest that across this time period, moderate coffee consumption can serve as some kind of protective factor against cognitive decline,” she added.

For tea, there was a somewhat different pattern. People who never drank tea had a greater decline in fluid intelligence, compared with those who had moderate consumption (beta, 0.06; SE, 0.02; P = .0090) or high consumption (beta, 0.06; SE, 0.02; P = .003).

Because this is an observational study, “we still need randomized controlled trials to better understand the neuroprotective mechanism of coffee and tea compounds,” said Dr. Sewell.

Responding later to a query from a meeting delegate about how moderate coffee drinking could be protective, Dr. Sewell said there are probably “different levels of mechanisms,” including at the molecular level (possibly involving amyloid toxicity) and the behavioral level (possibly involving sleep patterns).

Dr. Sewell said that she hopes this line of investigation will lead to new avenues of research in preventive strategies for Alzheimer’s disease. 

“We hope that coffee and tea intake could contribute to the development of a safe and inexpensive strategy for delaying the onset and reducing the incidence for Alzheimer’s disease.”

A limitation of the study is possible recall bias, because coffee and tea consumption were self-reported. However, this may not be much of an issue because coffee and tea consumption “is usually quite a habitual behavior,” said Dr. Sewell.

The study also had no data on midlife coffee or tea consumption and did not compare the effect of different preparation methods or types of coffee and tea — for example, green tea versus black tea. 

When asked if the study controlled for smoking, Dr. Sewell said it didn’t but added that it would be interesting to explore its impact on cognition.

Dr. Sewell reported no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

PHILADELPHIA – Drinking more than three cups of coffee a day is linked to more rapid cognitive decline over time, results from a large study suggest.

Investigators examined the impact of different amounts of coffee and tea on fluid intelligence — a measure of cognitive functions including abstract reasoning, pattern recognition, and logical thinking.

“It’s the old adage that too much of anything isn’t good. It’s all about balance, so moderate coffee consumption is okay but too much is probably not recommended,” said study investigator Kelsey R. Sewell, PhD, Advent Health Research Institute, Orlando, Florida. 

The findings of the study were presented at the 2024 Alzheimer’s Association International Conference (AAIC).
 

One of the World’s Most Widely Consumed Beverages

Coffee is one of the most widely consumed beverages around the world. The beans contain a range of bioactive compounds, including caffeine, chlorogenic acid, and small amounts of vitamins and minerals.

Consistent evidence from observational and epidemiologic studies indicates that intake of both coffee and tea has beneficial effects on stroke, heart failure, cancers, diabetes, and Parkinson’s disease.  

Several studies also suggest that coffee may reduce the risk for Alzheimer’s disease, said Dr. Sewell. However, there are limited longitudinal data on associations between coffee and tea intake and cognitive decline, particularly in distinct cognitive domains.

Dr. Sewell’s group previously published a study of cognitively unimpaired older adults that found greater coffee consumption was associated with slower cognitive decline and slower accumulation of brain beta-amyloid.

Their current study extends some of the prior findings and investigates the relationship between both coffee and tea intake and cognitive decline over time in a larger sample of older adults.

This new study included 8451 mostly female (60%) and White (97%) cognitively unimpaired adults older than 60 (mean age, 67.8 years) in the UK Biobank, a large-scale research resource containing in-depth, deidentified genetic and health information from half a million UK participants. Study subjects had a mean body mass index (BMI) of 26, and about 26% were apolipoprotein epsilon 4 (APOE e4) gene carriers.

Researchers divided coffee and tea consumption into tertiles: high, moderate, and no consumption.

For daily coffee consumption, 18% reported drinking four or more cups (high consumption), 58% reported drinking one to three cups (moderate consumption), and 25% reported that they never drink coffee. For daily tea consumption, 47% reported drinking four or more cups (high consumption), 38% reported drinking one to three cups (moderate consumption), and 15% reported that they never drink tea.

The study assessed cognitive function at baseline and at least two additional patient visits. 

Researchers used linear mixed models to assess the relationships between coffee and tea intake and cognitive outcomes. The models adjusted for age, sex, Townsend deprivation index (reflecting socioeconomic status), ethnicity, APOE e4 status, and BMI.
 

Steeper Decline 

Compared with high coffee consumption (four or more cups daily), people who never consumed coffee (beta, 0.06; standard error [SE], 0.02; P = .005) and those with moderate consumption (beta, 0.07; SE, 0.02; P = < .001) had slower decline in fluid intelligence after an average of 8.83 years of follow-up.

“We can see that those with high coffee consumption showed the steepest decline in fluid intelligence across the follow up, compared to those with moderate coffee consumption and those never consuming coffee,” said Dr. Sewell, referring to illustrative graphs.

At the same time, “our data suggest that across this time period, moderate coffee consumption can serve as some kind of protective factor against cognitive decline,” she added.

For tea, there was a somewhat different pattern. People who never drank tea had a greater decline in fluid intelligence, compared with those who had moderate consumption (beta, 0.06; SE, 0.02; P = .0090) or high consumption (beta, 0.06; SE, 0.02; P = .003).

Because this is an observational study, “we still need randomized controlled trials to better understand the neuroprotective mechanism of coffee and tea compounds,” said Dr. Sewell.

Responding later to a query from a meeting delegate about how moderate coffee drinking could be protective, Dr. Sewell said there are probably “different levels of mechanisms,” including at the molecular level (possibly involving amyloid toxicity) and the behavioral level (possibly involving sleep patterns).

Dr. Sewell said that she hopes this line of investigation will lead to new avenues of research in preventive strategies for Alzheimer’s disease. 

“We hope that coffee and tea intake could contribute to the development of a safe and inexpensive strategy for delaying the onset and reducing the incidence for Alzheimer’s disease.”

A limitation of the study is possible recall bias, because coffee and tea consumption were self-reported. However, this may not be much of an issue because coffee and tea consumption “is usually quite a habitual behavior,” said Dr. Sewell.

The study also had no data on midlife coffee or tea consumption and did not compare the effect of different preparation methods or types of coffee and tea — for example, green tea versus black tea. 

When asked if the study controlled for smoking, Dr. Sewell said it didn’t but added that it would be interesting to explore its impact on cognition.

Dr. Sewell reported no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

PHILADELPHIA – Drinking more than three cups of coffee a day is linked to more rapid cognitive decline over time, results from a large study suggest.

Investigators examined the impact of different amounts of coffee and tea on fluid intelligence — a measure of cognitive functions including abstract reasoning, pattern recognition, and logical thinking.

“It’s the old adage that too much of anything isn’t good. It’s all about balance, so moderate coffee consumption is okay but too much is probably not recommended,” said study investigator Kelsey R. Sewell, PhD, Advent Health Research Institute, Orlando, Florida. 

The findings of the study were presented at the 2024 Alzheimer’s Association International Conference (AAIC).
 

One of the World’s Most Widely Consumed Beverages

Coffee is one of the most widely consumed beverages around the world. The beans contain a range of bioactive compounds, including caffeine, chlorogenic acid, and small amounts of vitamins and minerals.

Consistent evidence from observational and epidemiologic studies indicates that intake of both coffee and tea has beneficial effects on stroke, heart failure, cancers, diabetes, and Parkinson’s disease.  

Several studies also suggest that coffee may reduce the risk for Alzheimer’s disease, said Dr. Sewell. However, there are limited longitudinal data on associations between coffee and tea intake and cognitive decline, particularly in distinct cognitive domains.

Dr. Sewell’s group previously published a study of cognitively unimpaired older adults that found greater coffee consumption was associated with slower cognitive decline and slower accumulation of brain beta-amyloid.

Their current study extends some of the prior findings and investigates the relationship between both coffee and tea intake and cognitive decline over time in a larger sample of older adults.

This new study included 8451 mostly female (60%) and White (97%) cognitively unimpaired adults older than 60 (mean age, 67.8 years) in the UK Biobank, a large-scale research resource containing in-depth, deidentified genetic and health information from half a million UK participants. Study subjects had a mean body mass index (BMI) of 26, and about 26% were apolipoprotein epsilon 4 (APOE e4) gene carriers.

Researchers divided coffee and tea consumption into tertiles: high, moderate, and no consumption.

For daily coffee consumption, 18% reported drinking four or more cups (high consumption), 58% reported drinking one to three cups (moderate consumption), and 25% reported that they never drink coffee. For daily tea consumption, 47% reported drinking four or more cups (high consumption), 38% reported drinking one to three cups (moderate consumption), and 15% reported that they never drink tea.

The study assessed cognitive function at baseline and at least two additional patient visits. 

Researchers used linear mixed models to assess the relationships between coffee and tea intake and cognitive outcomes. The models adjusted for age, sex, Townsend deprivation index (reflecting socioeconomic status), ethnicity, APOE e4 status, and BMI.
 

Steeper Decline 

Compared with high coffee consumption (four or more cups daily), people who never consumed coffee (beta, 0.06; standard error [SE], 0.02; P = .005) and those with moderate consumption (beta, 0.07; SE, 0.02; P = < .001) had slower decline in fluid intelligence after an average of 8.83 years of follow-up.

“We can see that those with high coffee consumption showed the steepest decline in fluid intelligence across the follow up, compared to those with moderate coffee consumption and those never consuming coffee,” said Dr. Sewell, referring to illustrative graphs.

At the same time, “our data suggest that across this time period, moderate coffee consumption can serve as some kind of protective factor against cognitive decline,” she added.

For tea, there was a somewhat different pattern. People who never drank tea had a greater decline in fluid intelligence, compared with those who had moderate consumption (beta, 0.06; SE, 0.02; P = .0090) or high consumption (beta, 0.06; SE, 0.02; P = .003).

Because this is an observational study, “we still need randomized controlled trials to better understand the neuroprotective mechanism of coffee and tea compounds,” said Dr. Sewell.

Responding later to a query from a meeting delegate about how moderate coffee drinking could be protective, Dr. Sewell said there are probably “different levels of mechanisms,” including at the molecular level (possibly involving amyloid toxicity) and the behavioral level (possibly involving sleep patterns).

Dr. Sewell said that she hopes this line of investigation will lead to new avenues of research in preventive strategies for Alzheimer’s disease. 

“We hope that coffee and tea intake could contribute to the development of a safe and inexpensive strategy for delaying the onset and reducing the incidence for Alzheimer’s disease.”

A limitation of the study is possible recall bias, because coffee and tea consumption were self-reported. However, this may not be much of an issue because coffee and tea consumption “is usually quite a habitual behavior,” said Dr. Sewell.

The study also had no data on midlife coffee or tea consumption and did not compare the effect of different preparation methods or types of coffee and tea — for example, green tea versus black tea. 

When asked if the study controlled for smoking, Dr. Sewell said it didn’t but added that it would be interesting to explore its impact on cognition.

Dr. Sewell reported no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

PHILADELPHIA – Nearly half of dementia cases worldwide could theoretically be prevented or delayed by eliminating 14 modifiable risk factors during an individual’s lifetime, a report from the Lancet Commission on dementia prevention, intervention, and care.

The report adds two new modifiable risk factors for dementia — high cholesterol and vision loss — to the 12 risk factors identified in the 2020 Lancet Commission report, which were linked to about 40% of all dementia cases. 

The original Lancet Commission report, published in 2017, identified nine modifiable risk factors that were estimated to be responsible for one third of dementia cases. 

“Our new report reveals that there is much more that can and should be done to reduce the risk of dementia. It’s never too early or too late to act, with opportunities to make an impact at any stage of life,” lead author Gill Livingston, MD, from University College London in England, said in a statement. 

The 57-page report was published online in The Lancet Neurology (to coincide with its presentation at the 2024 Alzheimer’s Association International Conference (AAIC).
 

‘Compelling’ New Evidence 

The 12 risk factors cited in the 2020 report are lower levels of education, hearing loss, hypertension, smoking, obesity, depression, physical inactivity, diabetes, excessive alcohol consumption, traumatic brain injury (TBI), air pollution, and social isolation. 

According to the authors of the current report, there is “new compelling evidence” that untreated vision loss and elevated low-density lipoprotein (LDL) cholesterol are also risk factors for dementia.

These two added risk factors are associated with 9% of all dementia cases — with an estimated 7% of cases caused by high LDL cholesterol from about age 40 years, and 2% of cases caused by untreated vision loss in later life, the authors said.

Out of all 14 risk factors, those tied to the greatest proportion of dementia in the global population are hearing impairment and high LDL cholesterol (7% each), along with less education in early life, and social isolation in later life (5% each), the report estimates. 

The new report also outlines 13 recommendations aimed at individuals and governments to help guard against dementia. They include preventing and treating hearing loss, vision loss, and depression; being cognitively active throughout life; using head protection in contact sports; reducing vascular risk factors (high cholesterol, diabetes, obesity, hypertension); improving air quality; and providing supportive community environments to increase social contact. 

Tara Spires-Jones, PhD, president of the British Neuroscience Association, emphasized that, while this research doesn’t directly link specific factors to dementia, it supports evidence that a healthy lifestyle — encompassing education, social activities, exercise, cognitive engagement, and avoiding head injuries and harmful factors for heart and lung health — can enhance brain resilience and prevent dementia.

In an interview, Heather M. Snyder, PhD, senior vice president of medical and scientific relations, Alzheimer’s Association, said: “Our brains are complex and what happens throughout our lives may increase or decrease our risk for dementia as we age. Protecting brain health as we age requires a comprehensive approach that includes discussions on diet, exercise, heart health, hearing, and vision.”

Also weighing in on the new report, Shaheen Lakhan, MD, PhD, neurologist and researcher based in Miami, Florida, said the addition of high cholesterol is “particularly noteworthy as it reinforces the intricate connection between vascular health and brain health — a link we’ve long suspected but can now target more effectively.”

As for vision loss, “it’s not just a matter of seeing clearly; it’s a matter of thinking clearly. Untreated vision loss can lead to social isolation, reduced physical activity, and cognitive decline,” said Dr. Lakhan. 
 

Dementia Is Not Inevitable

In his view, “the potential to prevent or delay nearly half of dementia cases by addressing these risk factors is nothing short of revolutionary. It shifts our perspective from viewing dementia as an inevitable part of aging to seeing it as a condition we can actively work to prevent,” Dr. Lakhan added.

He said the report’s emphasis on health equity is also important. 

“Dementia risk factors disproportionately affect socioeconomically disadvantaged groups and low- and middle-income countries. Addressing these disparities isn’t just a matter of fairness in the fight against dementia, equality in prevention is as important as equality in treatment,” Dr. Lakhan commented.

While the report offers hope, it also presents a challenge, he said. 

Implementing the recommended preventive measures requires a “coordinated effort from individuals, healthcare systems, and policymakers. The potential benefits, both in terms of quality of life and economic savings, make this effort not just worthwhile but imperative. Preventing dementia is not just a medical imperative — it’s an economic and humanitarian one,” Dr. Lakhan said. 

Masud Husain, PhD, with the University of Oxford in England, agreed. 

The conclusions in this report are “very important for all of us, but particularly for health policy makers and government,” he said. 

“If we did simple things well such as screening for some of the factors identified in this report, with adequate resources to perform this, we have the potential to prevent dementia on a national scale. This would be far more cost effective than developing high-tech treatments, which so far have been disappointing in their impacts on people with established dementia,” Dr. Husain said. 

The Lancet Commission was funded by University College London, Alzheimer’s Society, Alzheimer’s Research UK, and the Economic and Social Research Council. A complete list of author disclosures is available with the original article. Dr. Snyder, Dr. Lakhan, Dr. Husain and Dr. Spires-Jones have no relevant disclosures.

A version of this article appeared on Medscape.com.

PHILADELPHIA – Nearly half of dementia cases worldwide could theoretically be prevented or delayed by eliminating 14 modifiable risk factors during an individual’s lifetime, a report from the Lancet Commission on dementia prevention, intervention, and care.

The report adds two new modifiable risk factors for dementia — high cholesterol and vision loss — to the 12 risk factors identified in the 2020 Lancet Commission report, which were linked to about 40% of all dementia cases. 

The original Lancet Commission report, published in 2017, identified nine modifiable risk factors that were estimated to be responsible for one third of dementia cases. 

“Our new report reveals that there is much more that can and should be done to reduce the risk of dementia. It’s never too early or too late to act, with opportunities to make an impact at any stage of life,” lead author Gill Livingston, MD, from University College London in England, said in a statement. 

The 57-page report was published online in The Lancet Neurology (to coincide with its presentation at the 2024 Alzheimer’s Association International Conference (AAIC).
 

‘Compelling’ New Evidence 

The 12 risk factors cited in the 2020 report are lower levels of education, hearing loss, hypertension, smoking, obesity, depression, physical inactivity, diabetes, excessive alcohol consumption, traumatic brain injury (TBI), air pollution, and social isolation. 

According to the authors of the current report, there is “new compelling evidence” that untreated vision loss and elevated low-density lipoprotein (LDL) cholesterol are also risk factors for dementia.

These two added risk factors are associated with 9% of all dementia cases — with an estimated 7% of cases caused by high LDL cholesterol from about age 40 years, and 2% of cases caused by untreated vision loss in later life, the authors said.

Out of all 14 risk factors, those tied to the greatest proportion of dementia in the global population are hearing impairment and high LDL cholesterol (7% each), along with less education in early life, and social isolation in later life (5% each), the report estimates. 

The new report also outlines 13 recommendations aimed at individuals and governments to help guard against dementia. They include preventing and treating hearing loss, vision loss, and depression; being cognitively active throughout life; using head protection in contact sports; reducing vascular risk factors (high cholesterol, diabetes, obesity, hypertension); improving air quality; and providing supportive community environments to increase social contact. 

Tara Spires-Jones, PhD, president of the British Neuroscience Association, emphasized that, while this research doesn’t directly link specific factors to dementia, it supports evidence that a healthy lifestyle — encompassing education, social activities, exercise, cognitive engagement, and avoiding head injuries and harmful factors for heart and lung health — can enhance brain resilience and prevent dementia.

In an interview, Heather M. Snyder, PhD, senior vice president of medical and scientific relations, Alzheimer’s Association, said: “Our brains are complex and what happens throughout our lives may increase or decrease our risk for dementia as we age. Protecting brain health as we age requires a comprehensive approach that includes discussions on diet, exercise, heart health, hearing, and vision.”

Also weighing in on the new report, Shaheen Lakhan, MD, PhD, neurologist and researcher based in Miami, Florida, said the addition of high cholesterol is “particularly noteworthy as it reinforces the intricate connection between vascular health and brain health — a link we’ve long suspected but can now target more effectively.”

As for vision loss, “it’s not just a matter of seeing clearly; it’s a matter of thinking clearly. Untreated vision loss can lead to social isolation, reduced physical activity, and cognitive decline,” said Dr. Lakhan. 
 

Dementia Is Not Inevitable

In his view, “the potential to prevent or delay nearly half of dementia cases by addressing these risk factors is nothing short of revolutionary. It shifts our perspective from viewing dementia as an inevitable part of aging to seeing it as a condition we can actively work to prevent,” Dr. Lakhan added.

He said the report’s emphasis on health equity is also important. 

“Dementia risk factors disproportionately affect socioeconomically disadvantaged groups and low- and middle-income countries. Addressing these disparities isn’t just a matter of fairness in the fight against dementia, equality in prevention is as important as equality in treatment,” Dr. Lakhan commented.

While the report offers hope, it also presents a challenge, he said. 

Implementing the recommended preventive measures requires a “coordinated effort from individuals, healthcare systems, and policymakers. The potential benefits, both in terms of quality of life and economic savings, make this effort not just worthwhile but imperative. Preventing dementia is not just a medical imperative — it’s an economic and humanitarian one,” Dr. Lakhan said. 

Masud Husain, PhD, with the University of Oxford in England, agreed. 

The conclusions in this report are “very important for all of us, but particularly for health policy makers and government,” he said. 

“If we did simple things well such as screening for some of the factors identified in this report, with adequate resources to perform this, we have the potential to prevent dementia on a national scale. This would be far more cost effective than developing high-tech treatments, which so far have been disappointing in their impacts on people with established dementia,” Dr. Husain said. 

The Lancet Commission was funded by University College London, Alzheimer’s Society, Alzheimer’s Research UK, and the Economic and Social Research Council. A complete list of author disclosures is available with the original article. Dr. Snyder, Dr. Lakhan, Dr. Husain and Dr. Spires-Jones have no relevant disclosures.

A version of this article appeared on Medscape.com.

PHILADELPHIA – Nearly half of dementia cases worldwide could theoretically be prevented or delayed by eliminating 14 modifiable risk factors during an individual’s lifetime, a report from the Lancet Commission on dementia prevention, intervention, and care.

The report adds two new modifiable risk factors for dementia — high cholesterol and vision loss — to the 12 risk factors identified in the 2020 Lancet Commission report, which were linked to about 40% of all dementia cases. 

The original Lancet Commission report, published in 2017, identified nine modifiable risk factors that were estimated to be responsible for one third of dementia cases. 

“Our new report reveals that there is much more that can and should be done to reduce the risk of dementia. It’s never too early or too late to act, with opportunities to make an impact at any stage of life,” lead author Gill Livingston, MD, from University College London in England, said in a statement. 

The 57-page report was published online in The Lancet Neurology (to coincide with its presentation at the 2024 Alzheimer’s Association International Conference (AAIC).
 

‘Compelling’ New Evidence 

The 12 risk factors cited in the 2020 report are lower levels of education, hearing loss, hypertension, smoking, obesity, depression, physical inactivity, diabetes, excessive alcohol consumption, traumatic brain injury (TBI), air pollution, and social isolation. 

According to the authors of the current report, there is “new compelling evidence” that untreated vision loss and elevated low-density lipoprotein (LDL) cholesterol are also risk factors for dementia.

These two added risk factors are associated with 9% of all dementia cases — with an estimated 7% of cases caused by high LDL cholesterol from about age 40 years, and 2% of cases caused by untreated vision loss in later life, the authors said.

Out of all 14 risk factors, those tied to the greatest proportion of dementia in the global population are hearing impairment and high LDL cholesterol (7% each), along with less education in early life, and social isolation in later life (5% each), the report estimates. 

The new report also outlines 13 recommendations aimed at individuals and governments to help guard against dementia. They include preventing and treating hearing loss, vision loss, and depression; being cognitively active throughout life; using head protection in contact sports; reducing vascular risk factors (high cholesterol, diabetes, obesity, hypertension); improving air quality; and providing supportive community environments to increase social contact. 

Tara Spires-Jones, PhD, president of the British Neuroscience Association, emphasized that, while this research doesn’t directly link specific factors to dementia, it supports evidence that a healthy lifestyle — encompassing education, social activities, exercise, cognitive engagement, and avoiding head injuries and harmful factors for heart and lung health — can enhance brain resilience and prevent dementia.

In an interview, Heather M. Snyder, PhD, senior vice president of medical and scientific relations, Alzheimer’s Association, said: “Our brains are complex and what happens throughout our lives may increase or decrease our risk for dementia as we age. Protecting brain health as we age requires a comprehensive approach that includes discussions on diet, exercise, heart health, hearing, and vision.”

Also weighing in on the new report, Shaheen Lakhan, MD, PhD, neurologist and researcher based in Miami, Florida, said the addition of high cholesterol is “particularly noteworthy as it reinforces the intricate connection between vascular health and brain health — a link we’ve long suspected but can now target more effectively.”

As for vision loss, “it’s not just a matter of seeing clearly; it’s a matter of thinking clearly. Untreated vision loss can lead to social isolation, reduced physical activity, and cognitive decline,” said Dr. Lakhan. 
 

Dementia Is Not Inevitable

In his view, “the potential to prevent or delay nearly half of dementia cases by addressing these risk factors is nothing short of revolutionary. It shifts our perspective from viewing dementia as an inevitable part of aging to seeing it as a condition we can actively work to prevent,” Dr. Lakhan added.

He said the report’s emphasis on health equity is also important. 

“Dementia risk factors disproportionately affect socioeconomically disadvantaged groups and low- and middle-income countries. Addressing these disparities isn’t just a matter of fairness in the fight against dementia, equality in prevention is as important as equality in treatment,” Dr. Lakhan commented.

While the report offers hope, it also presents a challenge, he said. 

Implementing the recommended preventive measures requires a “coordinated effort from individuals, healthcare systems, and policymakers. The potential benefits, both in terms of quality of life and economic savings, make this effort not just worthwhile but imperative. Preventing dementia is not just a medical imperative — it’s an economic and humanitarian one,” Dr. Lakhan said. 

Masud Husain, PhD, with the University of Oxford in England, agreed. 

The conclusions in this report are “very important for all of us, but particularly for health policy makers and government,” he said. 

“If we did simple things well such as screening for some of the factors identified in this report, with adequate resources to perform this, we have the potential to prevent dementia on a national scale. This would be far more cost effective than developing high-tech treatments, which so far have been disappointing in their impacts on people with established dementia,” Dr. Husain said. 

The Lancet Commission was funded by University College London, Alzheimer’s Society, Alzheimer’s Research UK, and the Economic and Social Research Council. A complete list of author disclosures is available with the original article. Dr. Snyder, Dr. Lakhan, Dr. Husain and Dr. Spires-Jones have no relevant disclosures.

A version of this article appeared on Medscape.com.