Amyloid-β (β-amyloid)

Amyloid-β (Aβ) is a family of small protein fragments, 36 to 43 amino acids long. They are snipped out of a bigger protein (amyloid precursor protein, APP) by two enzymes (β- and γ-secretase). The 42-amino-acid version (Aβ42) is especially prone to misfolding. It clumps first into soluble 'oligomers', then into insoluble amyloid plaques. Those Aβ42 plaques are a defining feature of Alzheimer's disease. They show up on PET scans or in your spinal fluid years before symptoms. The 'amyloid cascade hypothesis' says Aβ buildup is the upstream trigger of Alzheimer's. But there is debate. Are the plaques themselves the main toxin, or a side effect? Most researchers now think the soluble oligomers, not the big fibrous plaques, are the most toxic form. Anti-amyloid antibody drugs have changed the picture. Lecanemab (FDA 2023, EMA 2025) and donanemab (FDA 2024) finished phase-3 trials and got approved. They modestly but significantly slowed cognitive decline while clearing a lot of plaque, lending qualified support to the cascade idea. An earlier drug, aducanumab (Aduhelm), got accelerated FDA approval in 2021 but Biogen withdrew it in January 2024 over commercial failure; it never got EMA approval.

Last reviewed: June 22, 2026

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