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Amyloid beta protein is a peptide of 36–43 amino acids derived from the proteolytic cleavage of amyloid precursor protein (APP) by β- and γ-secretases, with the most common forms being Aβ40 and Aβ42[7][3]. Aβ peptides are normally present in the brain, but their misfolding and accumulation into oligomers and amyloid fibrils are central to the pathology of Alzheimer’s disease[1][5]. This accumulation forms extracellular amyloid plaques, a key histopathological feature of AD[7]. Although Aβ itself is not a classic receptor, enzyme, or transporter, “Amyloid-beta protein accumulation” is a description of **pathological protein aggregation**, not a specific molecular entity, and should not be considered a canonical target name. However, Aβ is broadly considered the primary therapeutic target in AD, the focus of antibodies (e.g., aducanumab), anti-aggregation agents, and secretase inhibitors[2][4][6]. Note: - “Amyloid-beta protein accumulation” is not itself a molecule or receptor but rather a phenomenon/process. The preferred target entry should be “Amyloid beta protein (Aβ)” or its gene/protein precursor (APP), and not accumulation as an entity. For structured representation, "Amyloid beta protein" (Aβ) is the canonical name, and “accumulation” must not be part of the canonical field. - Therapeutic targeting focuses on either **lowering production, preventing aggregation, or promoting clearance** of amyloid beta protein[2][4]. - Amyloid-beta protein is not a receptor, enzyme, or transporter; it is an aggregation-prone peptide.
Monoclonal antibody-mediated clearance (phagocytosis and immune engagement), Inhibition of aggregation, Inhibition of β- or γ-secretases to reduce production, Immunotherapy (active and passive)
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