Fibrillar amyloid beta aggregate (Aβ fibril (or Abeta fibril))

Fibrillar amyloid beta aggregate is a **complex, insoluble protein aggregate** formed by the self-assembly and stabilization of amyloid-β (Aβ) peptide monomers into fibrils with a characteristic cross-β-sheet structure[1][2][3][4][5]. These fibrils are the principal component of the **amyloid plaques** found in the brains of individuals with Alzheimer’s disease and related conditions[1][4][7]. Fibrils are generated by the ordered stacking of Aβ peptide β-sheets perpendicular to the fibril axis, resulting in a highly stable, pathologic aggregate[5][6]. Amyloid-β fibrils constitute a major biomarker and a therapeutic target in Alzheimer’s disease, with a range of disease-modifying agents in development or approved that aim to clear these aggregates by immune or small-molecule means[4][5][7]. The accumulation of amyloid-β fibrils is implicated in neurodegeneration, synapse loss, and cognitive decline in affected disorders, although the direct causative relationship between fibrillar load and clinical impairment remains under investigation[5][6][7].

Other names

Amyloid-β fibrilAmyloid-beta fibrilsAmyloid beta fibrillar aggregateFibrillar amyloid-βAβ aggregate

Antibody-mediated clearance of amyloid plaques (passive immunotherapy); Inhibition of Aβ aggregation; Disaggregation or stabilization of non-fibrillar forms; Promotion of Aβ phagocytosis by microglia