Cellular and Molecular Signaling, Newark, NJ 07101, U.S.A.
Biochem Soc Trans. 2018 Apr 17;46(2):351-360. doi: 10.1042/BST20170121. Epub 2018 Mar 9.
As a result of the advancing age of the global population and the progressive increase in lifespan, neurodegenerative disorders continue to increase in incidence throughout the world. New strategies for neurodegenerative disorders involve the novel pathways of the mechanistic target of rapamycin (mTOR) and the silent mating-type information regulation 2 homolog 1 () (SIRT1) that can modulate pathways of apoptosis and autophagy. The pathways of mTOR and SIRT1 are closely integrated. mTOR forms the complexes mTOR Complex 1 and mTOR Complex 2 and can impact multiple neurodegenerative disorders that include Alzheimer's disease, Huntington's disease, and Parkinson's disease. SIRT1 can control stem cell proliferation, block neuronal injury through limiting programmed cell death, drive vascular cell survival, and control clinical disorders that include dementia and retinopathy. It is important to recognize that oversight of programmed cell death by mTOR and SIRT1 requires a fine degree of precision to prevent the progression of neurodegenerative disorders. Additional investigations and insights into these pathways should offer effective and safe treatments for neurodegenerative disorders.
由于全球人口老龄化和寿命的不断延长,世界各地的神经退行性疾病发病率持续上升。神经退行性疾病的新策略涉及雷帕霉素靶蛋白 (mTOR) 和沉默交配型信息调节 2 同源物 1 () (SIRT1) 的新途径,这些途径可以调节细胞凋亡和自噬途径。mTOR 和 SIRT1 途径密切相关。mTOR 形成 mTOR 复合物 1 和 mTOR 复合物 2,可影响多种神经退行性疾病,包括阿尔茨海默病、亨廷顿病和帕金森病。SIRT1 可以控制干细胞增殖,通过限制程序性细胞死亡来阻止神经元损伤,促进血管细胞存活,并控制包括痴呆症和视网膜病变在内的临床疾病。重要的是要认识到,mTOR 和 SIRT1 对程序性细胞死亡的监督需要高度精确,以防止神经退行性疾病的进展。对这些途径的进一步研究和深入了解应该为神经退行性疾病提供有效和安全的治疗方法。