A Glimmer of Hope: Maintain Mitochondrial Homeostasis to Mitigate Alzheimer's Disease.
A Glimmer of Hope: Maintain Mitochondrial Homeostasis to Mitigate Alzheimer's Disease.
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DOI：
10.14336/ad.2020.0105
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发表时间：
2020-10
影响因子：
7.4
通讯作者：
Tang M
中科院分区：
文献类型：
--
作者：
Li W;Kui L;Demetrios T;Gong X;Tang M
线粒体是传统上已知的细胞能量生产者。鉴于大脑中神经元的高能量需求性质，线粒体库保持健康并提供持续有效的能量供应至关重要。然而，线粒体功能障碍是不可避免的衰老和神经退行性疾病。在阿尔茨海默病（AD）中，神经元经历不平衡的稳态，如受损的线粒体生物发生和缺陷的线粒体自噬，后者促进疾病定义的淀粉样蛋白（Aβ）和p-Tau病理学，受损的线粒体自噬有助于炎症和含Aβ和p-Tau的神经毒性蛋白的聚集。因此，恢复有缺陷的线粒体自噬的干预措施可能会减轻AD症状，指出一种新疗法的可能性。这篇综述旨在说明线粒体生物学，重点是线粒体自噬，并提出治疗AD的策略，同时保持线粒体的稳态。
Mitochondria are classically known to be cellular energy producers. Given the high-energy demanding nature of neurons in the brain, it is essential that the mitochondrial pool remains healthy and provides a continuous and efficient supply of energy. However, mitochondrial dysfunction is inevitable in aging and neurodegenerative diseases. In Alzheimer’s disease (AD), neurons experience unbalanced homeostasis like damaged mitochondrial biogenesis and defective mitophagy, with the latter promoting the disease-defining amyloid β (Aβ) and p-Tau pathologies impaired mitophagy contributes to inflammation and the aggregation of Aβ and p-Tau-containing neurotoxic proteins. Interventions that restore defective mitophagy may, therefore, alleviate AD symptoms, pointing out the possibility of a novel therapy. This review aims to illustrate mitochondrial biology with a focus on mitophagy and propose strategies to treat AD while maintaining mitochondrial homeostasis.