Department of Neurology, Qingdao Municipal Hospital, Nanjing Medical University, Nanjing, China.
Mol Neurobiol. 2013 Dec;48(3):702-14. doi: 10.1007/s12035-013-8457-z. Epub 2013 Apr 27.
Autophagy is an essential and conserved lysosomal degradation pathway that controls the quality of cytoplasm by eliminating the intracellular aggregated proteins and damaged organelles. Autophagy works in mammalian target of rapamycin (mTOR)-dependent pathway or mTOR-independent pathway to keep the neuronal homeostasis. Mounting evidence has implicated the importance of defective autophagy in the pathogenesis of aging and neurodegenerative diseases, especially in Alzheimer's disease (AD). It has also demonstrated a neuroprotective role of autophagy in mediating the degradation of amyloid beta and tau which are major factors of AD. Amounts of molecules function in either mTOR-dependent pathway or mTOR-independent pathway to induce autophagy, which maybe a potential treatment for AD. In this review, we summarize the latest studies concerning the role of autophagy in AD and explore autophagy modulation as a potential therapeutic strategy for AD. However, to date, little of the researches on autophagy have been performed to investigate the modulation in AD; more investigations need to be confirmed in the future.
自噬是一种重要的、保守的溶酶体降解途径，通过清除细胞内聚集的蛋白质和受损的细胞器来控制细胞质的质量。自噬在哺乳动物雷帕霉素靶蛋白（mTOR）依赖性途径或 mTOR 非依赖性途径中发挥作用，以维持神经元的内稳态。越来越多的证据表明，自噬缺陷在衰老和神经退行性疾病的发病机制中很重要，特别是在阿尔茨海默病（AD）中。自噬在介导淀粉样β和tau 的降解中也具有神经保护作用，而淀粉样β和 tau 是 AD 的主要因素。大量分子在 mTOR 依赖性途径或 mTOR 非依赖性途径中发挥作用，诱导自噬，这可能是 AD 的一种潜在治疗方法。在这篇综述中，我们总结了关于自噬在 AD 中的作用的最新研究，并探讨了自噬调节作为 AD 的一种潜在治疗策略。然而，迄今为止，很少有关于自噬的研究来探讨 AD 中的调节；未来需要更多的研究来证实。
