Alzheimer's disease (AD) is the most common neurodegenerative disorder. The pathogenesis of AD is very complicated. For decades, the amyloid hypothesis has influenced and guided research in the field of AD. Meanwhile, researchers gradually realized that AD is caused by multiple concomitant factors, such as autophagy, mitochondrial quality control, insulin resistance and oxidative stress. In current clinical trials, the improvement strategies of AD, such as Aβ antibody immunotherapy and gamma secretase inhibitors, are limited. There is mounting evidence of neurodegenerative disorders indicated that activation of AMP-activated protein kinase (AMPK) may have broad neuroprotective effects. We reviewed the researches on AMPK for AD, the results demonstrated that activation of AMPK is controversial in Aβ deposition and tau phosphorylation, but is positive to promote autophagy, maintain mitochondrial quality control, reduce insulin resistance and relieve oxidative stress. It is concluded that AMPK might be a new target for AD by aggressively treating the risk factors in the future.

中文翻译：

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AMPK：阿尔茨海默氏病的潜在治疗靶标。

阿尔茨海默氏病（AD）是最常见的神经退行性疾病。AD的发病机制非常复杂。几十年来，淀粉样蛋白的假设影响和指导了AD领域的研究。同时，研究人员逐渐意识到AD是由多种伴随因素引起的，例如自噬，线粒体质量控制，胰岛素抵抗和氧化应激。在当前的临床试验中，AD的改善策略，例如Aβ抗体免疫疗法和γ分泌酶抑制剂，是有限的。越来越多的神经退行性疾病证据表明，AMP活化蛋白激酶（AMPK）的激活可能具有广泛的神经保护作用。我们回顾了AMPK用于AD的研究，结果表明AMPK的激活在Aβ沉积和tau磷酸化方面存在争议，但对促进自噬，维持线粒体质量控制，降低胰岛素抵抗和缓解氧化应激是积极的。结论是，通过在未来积极治疗风险因素，AMPK可能成为AD的新目标。