Beta-amyloid peptide (Aβ) (Aβ)

Beta-amyloid peptide aggregates are the hallmark pathological feature of Alzheimer's disease, forming extracellular senile plaques in the brain parenchyma (Source: NIH, PubMed). These peptides are generated through the sequential cleavage of the amyloid precursor protein (APP) by beta-secretase (BACE1) and gamma-secretase, producing fragments such as Aβ40 and the more aggregation-prone Aβ42 (Source: UniProt). While monomeric Aβ may play roles in synaptic signaling and antimicrobial defense, its transition into soluble oligomers and insoluble fibrils is associated with potent neurotoxicity, including synaptic loss and neuroinflammation (Source: PubMed). Therapeutic interventions, particularly monoclonal antibodies like lecanemab and aducanumab, target these aggregates to promote their clearance via microglial phagocytosis or to neutralize toxic species (Source: FDA). Despite their central role in Alzheimer's pathogenesis, targeting Aβ aggregates presents significant challenges, including the risk of amyloid-related imaging abnormalities (ARIA) and the need for early intervention before irreversible neuronal damage occurs (Source: StatPearls). The amyloid cascade hypothesis posits that the accumulation of these aggregates is the primary driver of the disease, triggering subsequent tau pathology and neurodegeneration (Source: PubMed).

Other names

Amyloid-betaA-betaAmyloid beta-peptideAβ40Aβ42Amyloid plaquesSenile plaquesBeta-amyloid peptide aggregatesAbeta

Monoclonal antibodies bind to specific epitopes on beta-amyloid monomers, oligomers, or fibrils to facilitate their clearance by microglia or to prevent the formation of toxic aggregates (Source: FDA, PubMed).