Amyloid beta monomer (Aβ monomer)

Amyloid beta monomer is a peptide of 38–43 amino acids produced by proteolytic cleavage of amyloid precursor protein (APP) via the amyloidogenic pathway[2][3][6]. In its monomeric form, amyloid beta (Aβ) is predominantly unstructured with rapid conformational interconversions, possessing little secondary structure in physiological solution; however, it can adopt more organized states under certain conditions[1][2][3][4]. Monomers can aggregate into oligomers and fibrils, the latter forming the amyloid plaques found in Alzheimer's disease brains[3][4][5]. While monomeric Aβ is associated with physiological roles such as antimicrobial activity, synaptic modulation, and barrier function, its misfolding and aggregation are considered central to Alzheimer's disease pathogenesis[2][5][6]. Current drug development targets aggregated, misfolded, or pathogenic forms of Aβ, including oligomers and fibrils, with monoclonal antibodies designed to modify disease progression in Alzheimer’s disease by enhancing clearance or neutralizing toxic species[2][3][6]. “Misfolded amyloid beta monomers” as a standalone therapeutic target is an imprecise concept, as toxicity is primarily ascribed to aggregated or oligomeric forms, but the conformational transition of the monomer is fundamental to the aggregation process[2][4][5]. **Note on is_incorrect:** The entry "Misfolded amyloid beta monomers" is not a standard or canonical therapeutic target name: classical nomenclature distinguishes between monomer, oligomer, and fibril forms of Aβ, and toxicity is commonly linked to oligomers and higher aggregates[2][3][4][5]. “Misfolded” monomer itself is not universally defined or recognized as a specific drug target, so the name is ambiguous and nonstandard for database or structured reference use[3][4][5].

Other names

Amyloid β-protein monomerAmyloid-β monomerAβ monomerAmyloid beta (Aβ)

Monoclonal antibodies bind and/or promote clearance of aggregated amyloid beta (including some that may bind monomeric or misfolded forms) - Inhibition of aggregation or promotion of clearance by modulating upstream enzymes (e.g., beta or gamma secretases, indirectly)