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BACE1 inhibition as a therapeutic strategy for Alzheimer's disease

Journal of Sport and Health Science 2016年第4期5卷 388-390页

作者： robert vassar Department of Cell and Molecular Biology The Feinberg School of MedicineNorthwestern University

*** identification ofβ-secretase asβ-site amyloid precursor protein cleaving enzyme（BACE）Following the discoveries ofβ-amyloid（Aβ）and the firs amyloid precursor protein（APP）mutations that cause familial Alzheimer’s disease（AD）,it soon became clear that theβ-andγ-secretase enzymes were prime therapeutic targets for the development of small-molecule inhibitor drugs for the treatment of AD.

关键词： BACE1

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现在与未来：阿尔茨海默病的诊断、预防和治疗策略（英文）

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Science Bulletin 2024年第23期 3777-3784页

作者：施炯 Jacques Touchon Lefkos T Middleton Mercé Boada Rovira robert vassar Bruno Vellas 申勇 Department of Neurology Institute on Aging and Brain Disorders the First Affiliated Hospital of USTC Division of Life Sciences and Medicine University of Science and Technology of China Neurodegenerative Disorder Research Center Division of Life Sciences and Medicine University of Science and Technology of China Institute of Neuroscience University Hospital Gui de Chauliac-Montpellier Ageing Epidemiology (AGE) Research School of Public Health Imperial College Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) Universitat International de Catalunya-Barcelona Department of Cell Biology Medical School Department of Neurology Feinberg School of Medicine Northwestern University IHU Health Age WHO Collaborating Center for Frailty Clinical & Geoscience Research and Geriatric Training Toulouse University Hospital INSERM UMR 1295 University Paul Sabatier

After a number of failed drug studies on Alzheimer’s disease (AD) over the past decade, clinical trials of AD started to show encouraging results and were approved or pending approval for clinical use. However,controversies on the clinically meaningful benefits and risks of brain edema and microhemorrhages have reminded us to think further about monitoring treatment and developing new drug targets. The goal of this review is to find insights from clinical trials that aimed at two key pathological features of AD, i.e.,amyloid-β (Aβ) and tau protein, and to explore other targets such as anti-inflammation in AD. The complex pathophysiology of AD may require combination therapies rather than monotherapy. Throughout the course of AD, multiple pathways are disrupted, presenting a multitude of possible therapeutic targets for designing prevention and intervention for AD.

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