Amyloid-beta aggregate (Aβ aggregate) (Aβ aggregate)

Amyloid-beta aggregates are extracellular accumulations of misfolded amyloid-beta peptides, primarily Aβ42 and Aβ40, which are derived from the proteolytic cleavage of the amyloid precursor protein (APP) (Source: UniProt P05067). These aggregates progress from soluble oligomers to insoluble fibrils and eventually form dense senile plaques, which are a hallmark pathological feature of Alzheimer's disease (Source: NIH National Institute on Aging). In the brain, these aggregates exert neurotoxic effects by disrupting synaptic signaling, inducing oxidative stress, and triggering chronic neuroinflammation through microglial activation (Source: PubMed, PMID: 27029513). As a therapeutic target, amyloid-beta aggregates are the focus of several monoclonal antibodies designed to reduce plaque burden and slow cognitive decline. Drugs like lecanemab and donanemab specifically target these aggregated forms to promote their clearance via the immune system (Source: FDA, Leqembi Prescribing Information). Despite their clinical utility, targeting these plaques is associated with safety risks such as amyloid-related imaging abnormalities (ARIA), which require careful monitoring during treatment (Source: PubMed, PMID: 33536018).

Other names

Amyloid-beta plaqueAβ plaqueSenile plaqueAmyloid-beta fibrilAmyloid-beta oligomerNeuritic plaque

Monoclonal antibodies bind to specific epitopes on amyloid-beta aggregates, protofibrils, or plaques, facilitating their clearance through microglial-mediated phagocytosis or preventing further peptide polymerization (Source: PubMed, PMID: 36630463).