Amyloid beta peptide (primarily Aβ40 and Aβ42 forms) (Aβ)

Amyloid beta peptide (Aβ) is a small fragment (36–43 amino acids) derived from the amyloid-beta precursor protein (APP) by sequential cleavage by beta-secretase and gamma-secretase. In Alzheimer’s disease, abnormal processing leads to accumulation and aggregation of Aβ in the extracellular space of the brain, forming insoluble amyloid plaques characterized by cross-β-sheet fibrils. While physiological roles remain uncertain (potentially in synaptic regulation, antimicrobial defense, and metal homeostasis), pathological aggregation is toxic to neurons through synaptic dysfunction and cell death. Amyloid beta plaques are a hallmark of Alzheimer’s disease, making Aβ a preeminent therapeutic target for anti-aggregation therapies, monoclonal antibodies, and secretase inhibitors. "Beta amyloid A4 protein plaques" is not the canonical designation; the molecule of interest is amyloid beta peptide, with the aggregate form known as amyloid beta plaque.

Other names

Beta-amyloidAmyloid betaAβAbetaAmyloid-beta precursor protein (APP) (precursor)Senile plaque (aggregate form)

Immunotherapy: monoclonal antibodies bind Aβ, promote clearance (Aducanumab, Lecanemab, Donanemab); Enzyme inhibition: beta-secretase (BACE) inhibitors block Aβ production; Aggregation blockers: prevent oligomerization and fibril formation (experimental)