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, results of a prospective, longitudinal cohort study suggest.
In the study, excessive daytime sleepiness (EDS) was associated with increased accumulation of beta-amyloid, an important biomarker of AD that manifests in early preclinical stages, wrote first author Diego Z. Carvalho, MD, and his colleagues at the Mayo Clinic, Rochester, Minn. The report was published online March 12 in JAMA Neurology.
“It remains unclear whether EDS is a result of greater sleep instability, synaptic or network overload, or neurodegeneration of wakefulness-promoting centers,” Dr. Carvalho and colleagues wrote in their report. “However, participants with EDS were more vulnerable to AD pathologic processes.”
The prospective, longitudinal cohort analysis from Dr. Carvalho and his colleagues included 283 participants age 70 or older without a diagnosis of dementia who filled out a sleepiness assessment survey and underwent baseline and follow-up imaging studies as part of the Mayo Clinic Study of Aging.
All participants included in the analysis underwent at least two consecutive carbon 11–labeled Pittsburgh compound B PET (PiB-PET) scans. EDS, defined as a score of at least 10 on the Epworth Sleepiness Scale, was seen in 63 participants (22.3%), the researchers found.
At baseline, EDS was significantly associated with increased beta-amyloid accumulation in the anterior cingulate (P = .04), posterior cingulate-precuneus (P = .02), and parietal (P = .04) regions. The association between EDS and longitudinal beta-amyloid accumulation was most pronounced in participants who had global PiB positivity at baseline in anterior cingulate and cingulate-precuneus regions (P = .02 for both), they reported.
Findings of the study are consistent with a previous investigation of middle-aged participants without dementia, Dr. Carvalho and coauthors said in a discussion of the results. In that study, increased daytime somnolence was associated with increased beta-amyloid burden in regions including the precuneus and anterior cingulate. Daytime sleepiness in that study was measured using a different measure, the Sleep Scale, which was originally developed as part of the Medical Outcomes Study.
Further investigation of the link between EDS and beta-amyloid accumulation is needed. In particular, the researchers suggested that future studies might evaluate whether amyloid accumulation can be avoided through early recognition of EDS and subsequent treatment of the underlying sleep disorder.
The study was funded by grants from the National Institutes of Health and several foundations. Dr. Carvalho reported no disclosures related to the study. Many of his coauthors reported relationships with a variety of pharmaceutical companies developing therapies for Alzheimer’s.
SOURCE: Carvalho D et al., JAMA Neurol. 2018 Mar 12. doi: 10.1001/jamaneurol.2018.0049
The study by Dr. Carvalho and his colleagues advances the understanding of sleep disturbance as a risk factor for Alzheimer’s disease.
Findings of the study suggest that poor sleep quality may be an early warning sign of AD-related processes, but we advise caution in interpreting the results of this prospective cohort study given that daytime sleepiness was assessed subjectively using the Epworth Sleepiness Scale (ESS), which may reflect declining sleep quality, but is not necessarily a warning sign for impending amyloidosis because of the low specificity of subjective sleepiness and the many underlying causes that could contribute to ESS scores.
Nevertheless, the results hint at a time in the future when sleep dysfunction might be managed with sleep-based interventions that are deployed at the most optimal time to intervene in the beta-amyloid cascade.
Future studies would ideally include other markers of AD progression, such as cortical atrophy, tau deposition, or cardiovascular changes, and better explain a physiologic link between subjective daytime sleepiness and longitudinal change in beta-amyloid.
Joseph R. Winer is with the department of psychology at the University of California, Berkeley, and Bryce A. Mander, PhD, is with the University of California, Irvine. The text above is derived from their editorial appearing in JAMA Neurology (2018 Mar 12. doi: 10.1001/jamaneurol.2018.0005). The authors reported no conflict of interest disclosures related to their editorial contribution.
The study by Dr. Carvalho and his colleagues advances the understanding of sleep disturbance as a risk factor for Alzheimer’s disease.
Findings of the study suggest that poor sleep quality may be an early warning sign of AD-related processes, but we advise caution in interpreting the results of this prospective cohort study given that daytime sleepiness was assessed subjectively using the Epworth Sleepiness Scale (ESS), which may reflect declining sleep quality, but is not necessarily a warning sign for impending amyloidosis because of the low specificity of subjective sleepiness and the many underlying causes that could contribute to ESS scores.
Nevertheless, the results hint at a time in the future when sleep dysfunction might be managed with sleep-based interventions that are deployed at the most optimal time to intervene in the beta-amyloid cascade.
Future studies would ideally include other markers of AD progression, such as cortical atrophy, tau deposition, or cardiovascular changes, and better explain a physiologic link between subjective daytime sleepiness and longitudinal change in beta-amyloid.
Joseph R. Winer is with the department of psychology at the University of California, Berkeley, and Bryce A. Mander, PhD, is with the University of California, Irvine. The text above is derived from their editorial appearing in JAMA Neurology (2018 Mar 12. doi: 10.1001/jamaneurol.2018.0005). The authors reported no conflict of interest disclosures related to their editorial contribution.
The study by Dr. Carvalho and his colleagues advances the understanding of sleep disturbance as a risk factor for Alzheimer’s disease.
Findings of the study suggest that poor sleep quality may be an early warning sign of AD-related processes, but we advise caution in interpreting the results of this prospective cohort study given that daytime sleepiness was assessed subjectively using the Epworth Sleepiness Scale (ESS), which may reflect declining sleep quality, but is not necessarily a warning sign for impending amyloidosis because of the low specificity of subjective sleepiness and the many underlying causes that could contribute to ESS scores.
Nevertheless, the results hint at a time in the future when sleep dysfunction might be managed with sleep-based interventions that are deployed at the most optimal time to intervene in the beta-amyloid cascade.
Future studies would ideally include other markers of AD progression, such as cortical atrophy, tau deposition, or cardiovascular changes, and better explain a physiologic link between subjective daytime sleepiness and longitudinal change in beta-amyloid.
Joseph R. Winer is with the department of psychology at the University of California, Berkeley, and Bryce A. Mander, PhD, is with the University of California, Irvine. The text above is derived from their editorial appearing in JAMA Neurology (2018 Mar 12. doi: 10.1001/jamaneurol.2018.0005). The authors reported no conflict of interest disclosures related to their editorial contribution.
, results of a prospective, longitudinal cohort study suggest.
In the study, excessive daytime sleepiness (EDS) was associated with increased accumulation of beta-amyloid, an important biomarker of AD that manifests in early preclinical stages, wrote first author Diego Z. Carvalho, MD, and his colleagues at the Mayo Clinic, Rochester, Minn. The report was published online March 12 in JAMA Neurology.
“It remains unclear whether EDS is a result of greater sleep instability, synaptic or network overload, or neurodegeneration of wakefulness-promoting centers,” Dr. Carvalho and colleagues wrote in their report. “However, participants with EDS were more vulnerable to AD pathologic processes.”
The prospective, longitudinal cohort analysis from Dr. Carvalho and his colleagues included 283 participants age 70 or older without a diagnosis of dementia who filled out a sleepiness assessment survey and underwent baseline and follow-up imaging studies as part of the Mayo Clinic Study of Aging.
All participants included in the analysis underwent at least two consecutive carbon 11–labeled Pittsburgh compound B PET (PiB-PET) scans. EDS, defined as a score of at least 10 on the Epworth Sleepiness Scale, was seen in 63 participants (22.3%), the researchers found.
At baseline, EDS was significantly associated with increased beta-amyloid accumulation in the anterior cingulate (P = .04), posterior cingulate-precuneus (P = .02), and parietal (P = .04) regions. The association between EDS and longitudinal beta-amyloid accumulation was most pronounced in participants who had global PiB positivity at baseline in anterior cingulate and cingulate-precuneus regions (P = .02 for both), they reported.
Findings of the study are consistent with a previous investigation of middle-aged participants without dementia, Dr. Carvalho and coauthors said in a discussion of the results. In that study, increased daytime somnolence was associated with increased beta-amyloid burden in regions including the precuneus and anterior cingulate. Daytime sleepiness in that study was measured using a different measure, the Sleep Scale, which was originally developed as part of the Medical Outcomes Study.
Further investigation of the link between EDS and beta-amyloid accumulation is needed. In particular, the researchers suggested that future studies might evaluate whether amyloid accumulation can be avoided through early recognition of EDS and subsequent treatment of the underlying sleep disorder.
The study was funded by grants from the National Institutes of Health and several foundations. Dr. Carvalho reported no disclosures related to the study. Many of his coauthors reported relationships with a variety of pharmaceutical companies developing therapies for Alzheimer’s.
SOURCE: Carvalho D et al., JAMA Neurol. 2018 Mar 12. doi: 10.1001/jamaneurol.2018.0049
, results of a prospective, longitudinal cohort study suggest.
In the study, excessive daytime sleepiness (EDS) was associated with increased accumulation of beta-amyloid, an important biomarker of AD that manifests in early preclinical stages, wrote first author Diego Z. Carvalho, MD, and his colleagues at the Mayo Clinic, Rochester, Minn. The report was published online March 12 in JAMA Neurology.
“It remains unclear whether EDS is a result of greater sleep instability, synaptic or network overload, or neurodegeneration of wakefulness-promoting centers,” Dr. Carvalho and colleagues wrote in their report. “However, participants with EDS were more vulnerable to AD pathologic processes.”
The prospective, longitudinal cohort analysis from Dr. Carvalho and his colleagues included 283 participants age 70 or older without a diagnosis of dementia who filled out a sleepiness assessment survey and underwent baseline and follow-up imaging studies as part of the Mayo Clinic Study of Aging.
All participants included in the analysis underwent at least two consecutive carbon 11–labeled Pittsburgh compound B PET (PiB-PET) scans. EDS, defined as a score of at least 10 on the Epworth Sleepiness Scale, was seen in 63 participants (22.3%), the researchers found.
At baseline, EDS was significantly associated with increased beta-amyloid accumulation in the anterior cingulate (P = .04), posterior cingulate-precuneus (P = .02), and parietal (P = .04) regions. The association between EDS and longitudinal beta-amyloid accumulation was most pronounced in participants who had global PiB positivity at baseline in anterior cingulate and cingulate-precuneus regions (P = .02 for both), they reported.
Findings of the study are consistent with a previous investigation of middle-aged participants without dementia, Dr. Carvalho and coauthors said in a discussion of the results. In that study, increased daytime somnolence was associated with increased beta-amyloid burden in regions including the precuneus and anterior cingulate. Daytime sleepiness in that study was measured using a different measure, the Sleep Scale, which was originally developed as part of the Medical Outcomes Study.
Further investigation of the link between EDS and beta-amyloid accumulation is needed. In particular, the researchers suggested that future studies might evaluate whether amyloid accumulation can be avoided through early recognition of EDS and subsequent treatment of the underlying sleep disorder.
The study was funded by grants from the National Institutes of Health and several foundations. Dr. Carvalho reported no disclosures related to the study. Many of his coauthors reported relationships with a variety of pharmaceutical companies developing therapies for Alzheimer’s.
SOURCE: Carvalho D et al., JAMA Neurol. 2018 Mar 12. doi: 10.1001/jamaneurol.2018.0049
FROM JAMA NEUROLOGY
Key clinical point: Elderly individuals who have excessive daytime sleepiness might be more susceptible to accumulation of beta-amyloid, an important biomarker of Alzheimer’s disease that manifests in early preclinical stages.
Major finding: Excessive daytime sleepiness was significantly associated with increased accumulation of beta-amyloid in the cingulate gyrus and precuneus regions (P = .02 for both brain regions).
Study details: A prospective, longitudinal, population-based study including 283 elderly participants without a diagnosis of dementia who filled out a sleepiness assessment survey and underwent imaging studies.
Disclosures: The study was funded by grants from the National Institutes of Health and several foundations. Many authors reported relationships with a variety of pharmaceutical companies developing therapies for Alzheimer’s.
Source: Carvalho D et al., JAMA Neurol. 2018 Mar 12. doi: 10.1001/jamaneurol.2018.0049.