中文摘要：

阿尔茨海默病（AD）是一种神经退行性疾病,Aβ的过量表达及异常堆积是其发生发展的主要原因之一.本文以β淀粉样蛋白级联假说为线索,阐述了α,β,γ分泌酶对Aβ生成的调节、不同形态Aβ的毒性以及Aβ毒性作用机制.不管是自主运动还是被动运动,中低强度有氧耐力运动均可通过抑制Aβ产生、促进其清除以及抑制其神经毒性作用来预防与缓解AD,但其具体分子生物学机制不甚清楚.因此还探讨了运动如何通过调节α,β,γ分泌酶之间的平衡抑制Aβ的产生;运动如何通过胞外降解、胞内吞噬、转运清除等途径促进Aβ清除;运动如何通过调控机体抗氧化能力、抗炎性反应、细胞凋亡等来抑制Aβ神经毒性.但抗阻运动对缓解AD病症是否仍具有积极意义,目前仍无相关动物实验证实.自噬是一种溶酶体依赖性降解代谢机制,在AD的发病进程中起到重要作用.研究发现,通过激活自噬可增强可溶性或纤维状Aβ的清除,但运动能否通过调控自噬水平促进脑内Aβ清除,也是今后需要解决的重要问题之一.

英文摘要：

Alzheimer＇s disease （AD） is a common ueurodegenerative disorder. The excessive expression and abnormal aggregation of amyloid-β peptide has been regarded as one of the main causes leading to development of Alzheimer＇ s disease. Based on amyloid-β cascade hypothesis, we expounded the regulation of α-, β-, γ-secretases in amyloid-β generation; reviewed the neurotoxicity of different aggregation states and toxicity mechanism of amyloid-β. Whether voluntary exercise or forced exercise, low intensity aerobic exercise could prevent from Alzheimer＇s disease by regulating amyloid-β, however, the mechanism was not clear. Therefore, this paper discussed that exercise inhibited amyloid-β generation by regulating α-, β-, γ-secretases ; exercise promoted amy- loid-β elimination with degradation, phagocytosis and clearance; exercise refrained amyloid-β neurotoxicity by regulating antioxidant, Anti-inflammation and apoptosis. However, there was no animal experiment that resistance exercise could play a positive effects to AD. Autophagy plays an important role in de- velopment of AD. Activation of autophagy could clear more soluble or fibrous amyloid-β. However, whether could autophagy suspend AD following exercise, which is a research emphasis in the future？