Amyloid-beta deposit (Aβ (or beta-amyloid))

Amyloid-beta deposit refers to extracellular aggregates predominantly consisting of amyloid-beta (Aβ) peptides (36–43 amino acids), which originate via cleavage of amyloid-beta precursor protein (APP) by β-secretase and γ-secretase. These deposits form amyloid plaques, a hallmark pathological feature of Alzheimer's disease, and are implicated in neurotoxicity, synaptic dysfunction, and neurodegeneration. There are multiple forms of Aβ, including soluble oligomers and insoluble fibrils, with the oligomeric species considered highly neurotoxic. The accumulation of amyloid-beta is central to the prevailing “amyloid cascade hypothesis” of Alzheimer’s pathogenesis. Therapeutic strategies include antibodies targeting Aβ aggregates, secretase inhibitors, and aggregation blockers, although significant safety and efficacy challenges remain. In addition to its pathological role, normal Aβ may participate in physiological processes such as antimicrobial defense, synaptic regulation, and injury response; thus, indiscriminate removal can have unintended consequences.

Other names

Amyloid-betabeta-amyloidAβbeta-amyloid depositscerebral amyloidneuritic plaques

Monoclonal antibodies bind to amyloid-beta aggregates or oligomers, facilitating immune-mediated clearance or direct disruption of aggregates (e.g., aducanumab, lecanemab, donanemab) Secretase inhibitors block production of Aβ from amyloid precursor protein (APP) Aggregation inhibitors prevent Aβ from forming toxic oligomers and fibrils Immunotherapies stimulate active or passive immunity against Aβ, enhancing clearance