RESEARCHERS from the University of Cincinnati, Ohio, suggest that increasing levels of the brain protein amyloid-β 42 (Aβ42) may slow cognitive decline in Alzheimer’s disease. While monoclonal antibody treatments have been developed to reduce amyloid plaques in the brain, a study group found that these drugs also unintentionally increase Aβ42, which may explain their cognitive benefits.
The research group was led by Alberto Espay, Professor of the James J. and Joan A. Gardner Center for Parkinson’s Disease at the University of Cincinnati. His research challenges the theory that amyloid plaques cause Alzheimer’s. This current study suggests that it’s the loss of soluble Aβ42, as opposed to plaque buildup, that contributes to Alzheimer’s progression. The data analyzed approximately 26,000 patients across 24 clinical trials and found that higher Aβ42 levels after treatment were linked to slower cognitive decline.
The findings align with Espay’s hypothesis that Aβ42 is crucial for neuron health, and increasing its levels could help preserve cognitive function. While the study highlights the potential of boosting Aβ42, it also raises questions about the current approach of reducing amyloid plaques. According to the authors, removing amyloid may harm the brain, potentially causing it to shrink faster after treatment.
These results highlight the need to explore therapies that directly raise Aβ42 levels without targeting amyloid plaques, providing a fresh perspective on Alzheimer’s treatment. This shift could lead to new drug development strategies aimed at preserving brain health while avoiding the negative effects of current treatments. These findings open the door to alternative approaches for managing Alzheimer’s, focusing on restoring Aβ42 levels rather than solely eliminating amyloid plaques.
Reference: Abanto J et al. Increases in amyloid-β42 slow cognitive and clinical decline in Alzheimer’s disease trials. Brain. 2024;awae216.
Anaya Malik | AMJ
