bétaamilloid

Beta-amyloid, often abbreviated as Aβ, is a peptide fragment derived from the amyloid precursor protein (APP). In the brain, APP is a transmembrane protein whose exact physiological function is still under investigation, though it is believed to play roles in neuronal growth, survival, and repair. Beta-amyloid is formed when APP is cleaved by enzymes called secretases. Specifically, it is produced by the sequential action of beta-secretase and gamma-secretase.

Beta-amyloid peptides can aggregate into various forms, including soluble oligomers and insoluble fibrils. These aggregates are a hallmark pathological feature of Alzheimer's disease. In Alzheimer's, beta-amyloid peptides accumulate in the brain and form plaques, which are extracellular deposits. The accumulation and aggregation of beta-amyloid are thought to be central to the neurodegenerative process in Alzheimer's disease, potentially leading to synaptic dysfunction and neuronal death.

Research into beta-amyloid is extensive, focusing on understanding its normal physiological role, the mechanisms of its aggregation, and its precise contribution to the pathogenesis of Alzheimer's disease. Therapeutic strategies for Alzheimer's disease often target the production, aggregation, or clearance of beta-amyloid, although clinical trials have yielded mixed results. The precise relationship between beta-amyloid and other pathological hallmarks of Alzheimer's, such as tau tangles, is an active area of scientific inquiry.