淀粉样前体蛋白
小胶质细胞
医学
神经保护
内分泌学
早老素
内科学
星形胶质细胞
体育锻炼
糖基化
阿尔茨海默病
疾病
老年斑
胰岛素降解酶
神经科学
受体
炎症
心理学
胰岛素
中枢神经系统
作者
Jing Zhang,Yunliang Guo,Yongxiang Wang,Lin Song,Rui Zhang,Yifeng Du
标识
DOI:10.1016/j.neulet.2017.12.025
摘要
Alzheimer’s disease (AD) is a devastating disease characterized with progressive neurodegenerative disorders in the elderly. Epidemiological and clinical studies reported that lifestyle factors could halt the progression of AD, especially physical exercise. In the present work, we investigated the effects of long-term treadmill exercise on the pathological cascades of AD in APP/PS1 mice. After exercise for 5 months, Aβ deposition was significantly ameliorated in terms of Aβ area fraction, plaque number and size. We also found that long-term treadmill exercise increased neuronal density and attenuated activation of astrocytes. However, the activation of microglia was not affected in APP/PS1 mice treated with exercise intervention. In addition, the amyloidogenic pathway of amyloid precursor protein (APP) metabolism was inhibited, with the decrease of β-site amyloid precursor protein cleaving enzyme 1 (BACE1) and presenilin 1 (PS1). Nevertheless, the nonamyloidogenic pathway of APP metabolism was increased after exercise intervention. The expression levels of insulin-degrading enzyme (IDE) and receptor for advanced glycation end products (RAGE) also declined significantly. In conclusion, long-term treadmill exercise is neuroprotective against Aβ burdens and astrocyte activation, which contributes to the therapy for AD.
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