Newly published research from Yale Pathology substantiates the impact of the drug aducanumab in reducing a plaque that is a defining pathologic feature of Alzheimer’s disease. The study was published in Acta Neuropathologica.
Plaques composed of amyloid beta are naturally occurring proteins, but in patients with Alzheimer’s disease, abnormal levels of amyloid beta band together to form plaques that gather between neurons and disrupt cell function. Aducanumab has been shown to reduce the number and size of amyloid beta plaques in patients with early signs of Alzheimer’s and mild forms of the disease.
The research study details the first autopsy report of Alzheimer’s disease neuropathology in a patient previously treated with aducanumab. The patient was an 84-year-old woman who progressed to moderate dementia before receiving aducanumab. The patient received 32 monthly doses of the drug.
Amyloid PET scans demonstrated robust reduction of plaques. The patient passed away in hospice care, four months after her last dose of aducanumab. While the postmortem examination confirmed neuropathologic changes from Alzheimer’s, the density and size of amyloid plaques appeared lower in the patient compared to a reference cohort of untreated patients.
“Taken together, this case report is the first to provide amyloid PET and neuropathologic evidence substantiating the impact of aducanumab to reduce (amyloid beta) plaque neuropathology in a patient with Alzheimer’s,” explained Anita Huttner, MD, Associate Professor of Pathology, Director of the Neuropathology Program at Yale School of Medicine, and senior author of the study. “Furthermore, this report underscores the critical importance of autopsy neuropathology studies to augment our understanding of aducanumab’s mechanism of action and impact on Alzheimer’s biomarkers.”
Funding for the study was provided by the National Institute on Aging. Christopher Van Dyck, MD, Professor of Psychiatry, Neurology, and Neuroscience; Director of the Yale Alzheimer’s Disease Research Center; Director of the Alzheimer’s Disease Research Unit; and Director of the Division of Aging and Geriatric Psychiatry at Yale School of Medicine, also collaborated on the research.