Amyloid-beta protein aggregate (Aβ) (Aβ)

Aggregated amyloid-beta (Aβ) plaques and fibrils are extracellular protein deposits primarily composed of Aβ peptides, which are cleavage products of the amyloid precursor protein (APP) (Hardy & Higgins, 1992). These aggregates are a hallmark pathological feature of Alzheimer's disease and are central to the amyloid cascade hypothesis, where their accumulation triggers neurotoxic events including tau hyperphosphorylation and synaptic loss (Jack et al., 2018). While monomeric Aβ may have physiological roles in synaptic plasticity, the aggregated forms—ranging from soluble oligomers to insoluble fibrils—interfere with neuronal signaling and induce chronic neuroinflammation. Therapeutic strategies targeting these aggregates include monoclonal antibodies like lecanemab and donanemab, which are designed to recognize and bind to specific conformational epitopes to promote plaque clearance via microglial phagocytosis (FDA, 2023). Clinical trials have demonstrated that reducing the amyloid burden can slow cognitive decline in early-stage Alzheimer's patients (van Dyck et al., 2023). However, these therapies are associated with Amyloid-Related Imaging Abnormalities (ARIA), which include brain edema and microhemorrhages, necessitating rigorous safety monitoring (Sperling et al., 2011).

Other names

Amyloid-beta plaquesAmyloid-beta fibrilsBeta-amyloidSenile plaquesNeuritic plaquesAβ42 aggregates

Binding to aggregated Aβ species to facilitate microglial phagocytosis and plaque removal (van Dyck et al., 2023; FDA, 2023).