COMMENTARY—Impressive Findings Provide Hope for Patients With CAA-ri

Using a sensitive new technique for measuring low levels of CSF anti-amyloid β (Aβ) antibodies, Piazza et al provide compelling evidence that cerebral amyloid angiopathy-related inflammation (CAA-ri), which is characterized by vasogenic edema and multiple cortical or subcortical microbleeds, may be mediated by these antibodies. Similar amyloid-related imaging abnormalities (ARIA) may be seen in a subset of patients with Alzheimer’s disease following passive immunization with Aβ antibodies.

The impressive findings by Piazza et al require further confirmation and additional evidence that Aβ antibodies play a primary role in CAA-ri pathogenesis, rather than being either a biologic marker or epiphenomenon. If the findings are confirmed, immunomodulating or immunosuppressive therapy might improve the prognosis of patients with CAA-ri. In addition, it would be important to explore the exciting possibility that low-level sensitive CSF Ab antibodies might contribute to the pathology of Alzheimer’s disease, particularly since there is growing evidence that inflammation and activation of the innate immune response may play a role in this disorder.

—Stuart D. Cook, MD
Ruth Dunietz Kushner and Michael Jay Serwitz Professor of Neurology and
Neurosciences, Rutgers, The State University of New Jersey, Newark

Using a sensitive new technique for measuring low levels of CSF anti-amyloid β (Aβ) antibodies, Piazza et al provide compelling evidence that cerebral amyloid angiopathy-related inflammation (CAA-ri), which is characterized by vasogenic edema and multiple cortical or subcortical microbleeds, may be mediated by these antibodies. Similar amyloid-related imaging abnormalities (ARIA) may be seen in a subset of patients with Alzheimer’s disease following passive immunization with Aβ antibodies.

The impressive findings by Piazza et al require further confirmation and additional evidence that Aβ antibodies play a primary role in CAA-ri pathogenesis, rather than being either a biologic marker or epiphenomenon. If the findings are confirmed, immunomodulating or immunosuppressive therapy might improve the prognosis of patients with CAA-ri. In addition, it would be important to explore the exciting possibility that low-level sensitive CSF Ab antibodies might contribute to the pathology of Alzheimer’s disease, particularly since there is growing evidence that inflammation and activation of the innate immune response may play a role in this disorder.

—Stuart D. Cook, MD
Ruth Dunietz Kushner and Michael Jay Serwitz Professor of Neurology and
Neurosciences, Rutgers, The State University of New Jersey, Newark

Using a sensitive new technique for measuring low levels of CSF anti-amyloid β (Aβ) antibodies, Piazza et al provide compelling evidence that cerebral amyloid angiopathy-related inflammation (CAA-ri), which is characterized by vasogenic edema and multiple cortical or subcortical microbleeds, may be mediated by these antibodies. Similar amyloid-related imaging abnormalities (ARIA) may be seen in a subset of patients with Alzheimer’s disease following passive immunization with Aβ antibodies.

The impressive findings by Piazza et al require further confirmation and additional evidence that Aβ antibodies play a primary role in CAA-ri pathogenesis, rather than being either a biologic marker or epiphenomenon. If the findings are confirmed, immunomodulating or immunosuppressive therapy might improve the prognosis of patients with CAA-ri. In addition, it would be important to explore the exciting possibility that low-level sensitive CSF Ab antibodies might contribute to the pathology of Alzheimer’s disease, particularly since there is growing evidence that inflammation and activation of the innate immune response may play a role in this disorder.

—Stuart D. Cook, MD
Ruth Dunietz Kushner and Michael Jay Serwitz Professor of Neurology and
Neurosciences, Rutgers, The State University of New Jersey, Newark