Scientists have discovered two brain receptors, SST1 and SST4, that regulate the breakdown of amyloid beta, a protein linked to Alzheimer's disease. Activating these receptors increases neprilysin levels, reduces amyloid plaques, and improves memory in models, suggesting a potential new, safer, and less expensive treatment approach compared to current antibody therapies.
The muscle hormone irisin, which is elevated during exercise, has shown potential in reducing amyloid beta deposits, a hallmark of Alzheimer's disease (AD). Researchers used 3D cell models of AD and found that irisin treatment led to a significant reduction in amyloid beta pathology by increasing levels of neprilysin, an enzyme responsible for breaking down amyloid beta. The study also identified the receptor, integrin αV/β5, on astrocytes that irisin binds to, triggering the release of neprilysin. These findings suggest that irisin-based therapies could be a potential treatment for AD in the future.