JBC：运动疗法缓解阿尔茨海默氏症或更有效

日本京都大学一个研究小组日前说，他们通过动物实验发现，比起饮食疗法，运动疗法对改善阿尔茨海默氏症的记忆障碍更加有效。相关论文已经刊登在新一期《生物化学杂志》上。

阿尔茨海默氏症又称早老性痴呆症，临床症状为认知、记忆和语言功能障碍等。被认为是β淀粉样蛋白在脑内蓄积引起的，这与高脂肪食物有一定关联。

研究小组通过基因操作获得患有阿尔茨海默氏症的实验鼠，并让它们记住在水槽中游泳的路径，然后连续５个月喂食脂肪含量在６０％的高脂肪食物，在后两个半月里让一部分实验鼠在仓鼠轮子里运动，另一部分则不经常运动。

游泳测试发现，吃高脂肪食物的实验鼠中，没有经常运动的需要花费约３５秒才能游到终点，经常运动的只需要１６秒，脑内β淀粉样蛋白的蓄积比不运动的少约５０％。

另外一组对比实验发现，如果实验鼠不运动，但一直吃脂肪含量只有１０％的普通食物，游泳测试需要约２５秒，而吃普通食物并保持运动的实验鼠需要约１７秒。

因此，吃高脂肪食物的实验鼠，只要保持运动，记忆力也达到了吃普通食物实验鼠的水平。只控制饮食脂肪含量、但不运动的实验鼠，记忆力则明显不如保持运动的实验鼠。

doi:10.1074/jbc.M112.367011
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Exercise is more effective than diet control in preventing high fat diet-induced β-amyloid deposition and memory deficit in amyloid precursor protein transgenic mice

Masato Maesako1, Kengo Uemura2, Masakazu Kubota2, Akira Kuzuya2, Kazuki Sasaki2, Naoko Hayashida2, Megumi Asada-Utsugi2, Kiwamu Watanabe2, Maiko Uemura2, Takeshi Kihara2, Ryosuke Takahashi3, Shun Shimohama4 and Ayae Kinoshita

Accumulating evidence suggests that some dietary patterns, specifically high fat diet (HFD), increase the risk of developing sporadic Alzheimer disease (AD). Thus, interventions targeting HFD-induced metabolic dysfunctions may be effective in preventing the development of AD. We previously demonstrated that amyloid precursor protein (APP)-overexpressing transgenic mice fed HFD showed worsening of cognitive function compared to control APP mice on normal diet. Moreover, we reported that voluntary exercise ameliorates HFD-induced memory impairment and β-amyloid (Aβ) deposition. In the present study, we conducted diet control to ameliorate the metabolic abnormality caused by HFD on APP transgenic mice and compared the effect of diet control on cognitive function to that of voluntary exercise as well as that of combined (diet control plus exercise) treatment. Surprisingly, we found that exercise was more effective than diet control, although both exercise and diet control ameliorated HFD-induced memory deficit and Aβ deposition. The production of Aβ was not different between the exercise- and the diet control-treated mice. On the other hand, exercise specifically strengthened the activity of neprilysin, the Aβ degrading enzyme, the level of which was significantly correlated with that of deposited Aβ in our mice. Notably, the effect of the combination treatment (exercise and diet control) on memory and amyloid pathology was not significantly different from that of exercise alone. These studies provide solid evidence that exercise is a useful intervention to rescue HFD-induced aggravation of cognitive decline in transgenic model mice of AD.