运动可降低阿尔茨海默病大鼠模型海马中的 BACE 和 APP 水平。
Exercise decreases BACE and APP levels in the hippocampus of a rat model of Alzheimer's disease.
机构信息
Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX, USA.
Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX, USA.
出版信息
Mol Cell Neurosci. 2018 Jan;86:25-29. doi: 10.1016/j.mcn.2017.11.008. Epub 2017 Nov 9.
We investigated the effect of treadmill exercise training on the levels of Alzheimer's disease (AD)-related protein molecules in the DG and CA1 areas of a rat model of AD, i.c.v. infusion of Aβ1-42 peptide, 2weeks (250pmol/day). Aβ infusion markedly increased protein levels of amyloid precursor protein (APP), the secretase beta-site APP cleaving enzyme-1 (BACE-1) and Aβ in the CA1 and DG areas. The results also revealed that 4weeks of treadmill exercise prevented the increase in the levels of APP, BACE-1 and Aβ proteins in both hippocampal areas. Exercise, however, did not affect the levels of these proteins in normal rats. We suggest that exercise might be changing the equilibrium of APP processing pathway towards the nonpathogenic pathway most probably via increasing BDNF levels in the brain of AD model.
我们研究了跑步机运动训练对 AD 相关蛋白分子在 AD 大鼠模型 DG 和 CA1 区水平的影响，即侧脑室注射 Aβ1-42 肽，2 周（250pmol/天）。Aβ 输注显著增加了 CA1 和 DG 区淀粉样前体蛋白（APP）、β 位淀粉样前体蛋白裂解酶-1（BACE-1）和 Aβ 的蛋白水平。结果还表明，4 周的跑步机运动可防止 APP、BACE-1 和 Aβ 蛋白在两个海马区水平的增加。然而，运动对正常大鼠这些蛋白水平没有影响。我们认为，运动可能通过增加 AD 模型大脑中的脑源性神经营养因子（BDNF）水平，使 APP 加工途径的平衡向非致病途径转变。
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