WASHINGTON (dpa-AFX) - A recent study suggests that increasing the protein amyloid beta (Aß42) in the brain could help slow the progression of Alzheimer's disease.
Traditionally, the buildup of the protein called Aß42 has been considered the primary theory behind Alzheimer's, forming amyloid plaques around brain cells. However, researchers from the University of Cincinnati are proposing that Alzheimer's might stem from low levels of functional Aß42.
Alberto Espay, a neurology professor at the University of Cincinnati Academic Health Center, explained that Aß42 plays a protective role for the brain against various toxic and infectious threats. In its effort to combat these threats, Aß42 can convert into amyloid plaques, made up of aggregated Aß42 that no longer serves its protective function.
Espay and his team reviewed data from 26,000 participants involved in 24 randomized clinical trials assessing new treatments for Alzheimer's. They monitored cognitive function and Aß42 levels before and after treatment. The analysis revealed that patients who maintained higher levels of Aß42 post-treatment experienced slower cognitive decline.
Espay noted that individuals with amyloid plaques remain cognitively stable when they can generate sufficient Aß42 to keep it at normal levels. This conclusion is supported by the observation that recent antibody medications, such as lecanemab (Leqembi) and donanemab (Kisunla), inadvertently raised Aß42 levels in the brain. The data suggests that restoring Aß42 to normal levels could be more advantageous for Alzheimer's patients than merely removing amyloid plaques.
These insights may pave the way for new treatment strategies for Alzheimer's. Espay remarked that if Alzheimer's is linked to the loss of normal Aß42, increasing its levels could prove beneficial. Moving forward, the research team intends to explore treatments aimed at directly boosting Aß42 levels without focusing on amyloid targets.
Copyright(c) 2024 RTTNews.com. All Rights Reserved
Copyright RTT News/dpa-AFX
© 2024 AFX News
