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Targeting amyloid-β in Alzheimer's disease: A critical analysis of clinical trials and their implications for drug development
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DOI：10.22038/ijbms.2026.92189.19902.png)
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Abstract
En 中文
Alzheimer's disease (AD), a prevalent neurodegenerative dementia, is characterized by amyloid-(3 (A(3) plaques and neurofibrillary tangles, with A(3 playing a central pathogenic role. Approved AD drugs, primarily acetylcholinesterase inhibitors, only alleviate symptoms without modifying disease progression. A(3-targeting strategies aim to inhibit A(3 production or enhance its clearance, leveraging early deposition for proactive intervention. Preclinical studies show A(3 reduction mitigates neurodegeneration, but clinical trials reveal challenges: y-secretase inhibitors face off-target toxicities and limited efficacy, while BACE1 inhibitors suffer from safety issues or failure to improve cognition. Despite setbacks, advancing understanding of AD pathogenesis and optimized drug design/ trial protocols sustain the potential of A(3-targeted therapies. This review aims to advance A(3-targeted therapies for AD by integrating lessons from prior clinical trials and outlining strategic directions for future research and development.
Keywords:
gamma-Secretase
amyloid-beta
Alzheimer's disease
APP
BACE1
Small-molecule drugs
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