New study challenges Alzheimer's treatment theory by linking cognition to amyloid-beta levels

New research from the University of Cincinnati challenges the long-standing amyloid cascade hypothesis in Alzheimer's treatment. It suggests that increasing levels of amyloid-beta 42 (Aβ42) may improve cognition, rather than just reducing amyloid plaques. The study analyzed data from 24 clinical trials involving nearly 26,000 patients. It found that higher Aβ42 levels were linked to better cognitive outcomes, while treatments that lowered Aβ42 worsened performance. This indicates that Aβ42 may play a crucial role in brain health. Researchers propose that amyloid plaques might not directly cause Alzheimer's symptoms. Instead, the depletion of soluble Aβ42 could be a key factor in cognitive decline. Future studies may explore ways to increase Aβ42 levels without the risks associated with current treatments.