Amyloid-beta peptide (Aβ) (Aβ)

Amyloid-beta (Aβ) fibrils and plaques are extracellular protein aggregates primarily composed of 38-42 amino acid peptides derived from the proteolytic cleavage of the amyloid precursor protein (APP) by beta- and gamma-secretases (nih.gov, 2024). These aggregates are a defining pathological hallmark of Alzheimer's disease and are thought to play a central role in neurodegeneration according to the amyloid cascade hypothesis (wikipedia.org, 2025). While soluble Aβ monomers may have physiological roles in antimicrobial defense, synaptic regulation, and blood-brain barrier repair, their transition into oligomers, protofibrils, and eventually insoluble fibrils leads to the formation of senile plaques (frontiersin.org, 2018; mdpi.com, 2023). These plaques disrupt neuronal communication, induce oxidative stress, and trigger neuroinflammatory responses that contribute to cognitive decline (researchgate.net, 2024). Therapeutic strategies targeting these aggregates include monoclonal antibodies such as aducanumab, lecanemab, and donanemab, which are designed to bind to aggregated Aβ and facilitate its clearance via microglial-mediated phagocytosis (neurologylive.com, 2022; patsnap.com, 2026). Despite their potential to slow disease progression, these treatments are associated with significant safety concerns, most notably Amyloid-Related Imaging Abnormalities (ARIA), which include brain edema and microhemorrhages (nih.gov, 2022).

Other names

Amyloid-betaBeta-amyloidAbetaSenile plaquesNeuritic plaquesAmyloid-beta aggregatesAmyloid-beta fibrils

Passive immunotherapy involving monoclonal antibodies that bind to aggregated forms of amyloid-beta (such as oligomers, protofibrils, and plaques) to facilitate their clearance via microglial-mediated phagocytosis and direct dissociation of fibrils.