Amyloid-beta (Aβ) fibril (Aβ fibril)

Fibrillar amyloid-beta aggregates are the primary constituents of extracellular senile plaques and vascular deposits in the brains of patients with Alzheimer's disease and cerebral amyloid angiopathy [12, 17, 23]. These aggregates form through the misfolding and polymerization of amyloid-beta monomers, particularly the Aβ42 isoform, into insoluble beta-sheet rich structures [16, 24, 27]. While the physiological role of the amyloid-beta monomer remains debated, the fibrillar forms are associated with neurotoxicity, synaptic dysfunction, and the triggering of neuroinflammatory responses [13, 14, 20, 28]. Therapeutic strategies targeting these aggregates involve monoclonal antibodies designed to recognize specific epitopes on the fibrils or plaques to promote their clearance by the immune system [9, 10, 18]. Reducing the plaque burden is a key clinical objective aimed at slowing cognitive decline in early-stage Alzheimer's patients [1, 13, 22]. Notable safety concerns include amyloid-related imaging abnormalities (ARIA), which require careful monitoring via MRI during treatment [1}

Other names

Amyloid-beta plaqueSenile plaqueNeuritic plaqueAβ aggregateβ-amyloid fibrilAlzheimer amyloid fibrilCerebral amyloid angiopathy (CAA) depositVascular amyloid deposit

Monoclonal antibodies bind to fibrillar aggregates to facilitate clearance via microglial-mediated phagocytosis or direct dissolution of plaques [9, 10, 18, 20].