Amyloid beta aggregated form (Aβ (for Amyloid beta))

Amyloid beta aggregated forms refer to assemblies of the amyloid beta (Aβ) peptide, which are produced from amyloid precursor protein (APP) via sequential proteolytic cleavage. In their aggregated form, Aβ peptides exist as soluble oligomers, protofibrils, and insoluble fibrils, which in turn are the primary component of amyloid plaques found in the brains of individuals with Alzheimer’s disease[1][3][5][8]. The most studied isoforms are Aβ(1-40) and Aβ(1-42), with the latter being more prone to aggregate and exert neurotoxic effects[3][5][7]. Aβ aggregates disrupt cell membranes, interfere with synaptic function, and induce neuroinflammation, contributing critically to neurodegeneration and cognitive impairment in Alzheimer's disease[1][5][8]. Therapeutic strategies target these aggregated forms to prevent their formation, promote their clearance, or block their neurotoxic effects. Detection of aggregated Aβ in brain or CSF serves as a key biomarker for Alzheimer’s diagnosis and progression[8]. Early hopes that aggregated Aβ could be removed to reverse dementia have been tempered by the recognition of physiological roles of monomeric Aβ, as well as challenges related to safety, efficacy, and appropriate patient selection[2][4][6][8].

Other names

Amyloid beta aggregateAmyloid-beta oligomerAmyloid-beta fibrilAβ aggregateAβ oligomerAβ fibrilBeta-amyloid aggregateSenile plaque (in context of Alzheimer’s disease)

Antibody binding and clearance of aggregated amyloid beta by immune-mediated mechanisms (e.g., microglial phagocytosis); Inhibition of aggregation (small molecule or peptide inhibitors); Prevention of oligomer/fibril formation; Disruption or destabilization of amyloid plaques