Boosting brain protein may slow Alzheimer’s progression, study finds

A recent study conducted by researchers at the University of Cincinnati suggests that increasing levels of a specific brain protein, amyloid-beta 42 (Aβ42), may help slow the progression of Alzheimer’s disease. Traditionally, it has been believed that the accumulation of amyloid plaques in the brain is a primary cause of cognitive decline associated with Alzheimer’s. However, this study challenges that notion by indicating that higher levels of Aβ42 could be linked to slower cognitive impairment in patients treated with new monoclonal antibody medications, such as lecanemab and donanemab. The researchers observed that these medications, designed to eliminate amyloid plaques, inadvertently raised Aβ42 levels in the brain. This increase was associated with a deceleration in cognitive decline, suggesting that restoring Aβ42 to normal levels might be more beneficial than merely focusing on plaque removal. The findings imply that amyloid plaques may not be as harmful as previously thought, serving instead as indicators of the brain's response to stressors. Dr. Ozama Ismail from the Alzheimer’s Association emphasized the complexity of Alzheimer’s disease, noting that it is unlikely to be driven by a single biological mechanism. He advocates for a multifaceted approach to treatment that considers various underlying biological factors. This perspective aligns with the study's findings, which call for further investigation into therapies that boost Aβ42 levels without removing amyloid plaques. Overall, the study opens new avenues for Alzheimer’s research and treatment, suggesting that a shift in focus towards enhancing Aβ42 levels could lead to more effective strategies for managing the disease.