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Intermittent fasting promotes adult hippocampal neuronal differentiation by activating GSK-3β in 3xTg-AD mice.
Journal of Neurochemistry ( IF 4.2 ) Pub Date : 2020-06-23 , DOI: 10.1111/jnc.15105 Wei Li 1, 2 , Meijian Wu 1 , Yilin Zhang 1 , Xuemin Wei 1 , Jiankun Zang 1 , Yinghua Liu 3 , Yanping Wang 1 , Cheng-Xin Gong 4 , Wei Wei 1
Journal of Neurochemistry ( IF 4.2 ) Pub Date : 2020-06-23 , DOI: 10.1111/jnc.15105 Wei Li 1, 2 , Meijian Wu 1 , Yilin Zhang 1 , Xuemin Wei 1 , Jiankun Zang 1 , Yinghua Liu 3 , Yanping Wang 1 , Cheng-Xin Gong 4 , Wei Wei 1
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Moderate dietary restriction can ameliorate age‐related chronic diseases such as Alzheimer's disease (AD) by increasing the expression of neurotrophic factors and promoting neurogenesis in the brain. Glycogen synthase kinase‐3β (GSK‐3β) signaling is essential for the coordination of progenitor cell proliferation and differentiation during brain development. The mechanisms by which GSK‐3β is involved in dietary restriction‐induced neurogenesis and cognitive improvement remain unclear. Six‐month‐old male 3xTg‐AD and wild‐type mice were fed on alternate days (intermittent fasting, IF) or ad libitum (AL) for 3 months. GSK‐3β activity was regulated by bilaterally infusing lentiviral vectors carrying siRNA targeting GSK‐3β into the dentate gyrus region of the hippocampus. Intermittent fasting promoted neuronal differentiation and maturation in the dentate gyrus and ameliorated recognized dysfunction in 3xTg‐AD mice. These effects were reversed by siRNA targeting GSK‐3β. After intermittent fasting, the insulin and protein kinase A signaling pathways were inhibited, while the adenosine monophosphate‐activated protein kinase and brain‐derived neurotrophic factor pathways were activated. These findings suggest that intermittent fasting can promote neuronal differentiation and maturation in the hippocampus by activating GSK‐3β, thus improving learning and memory.
中文翻译：
间歇性禁食通过激活3xTg-AD小鼠中的GSK-3β来促进成年海马神经元分化。
适度的饮食限制可通过增加神经营养因子的表达并促进大脑中的神经发生而改善与年龄有关的慢性疾病，例如阿尔茨海默氏病（AD）。糖原合酶激酶-3β（GSK-3β）信号对于协调大脑发育过程中祖细胞的增殖和分化至关重要。GSK-3β参与饮食限制诱导的神经发生和认知改善的机制仍不清楚。六个月大的雄性3xTg-AD和野生型小鼠隔天（间歇禁食，IF）或随意（AL）喂养3个月。GSK-3β活性是通过将靶向GSK-3β的siRNA的慢病毒载体双向注入海马的齿状回区域来调节的。间歇性禁食可促进3xTg-AD小鼠的齿状回神经元分化和成熟，并改善公认的功能障碍。通过靶向GSK-3β的siRNA可以逆转这些作用。间歇性禁食后，胰岛素和蛋白激酶A信号通路被抑制，而腺苷一磷酸激活的蛋白激酶和脑源性神经营养因子通路被激活。这些发现表明，间歇性禁食可以通过激活GSK-3β促进海马神经元的分化和成熟，从而改善学习和记忆能力。而腺苷一磷酸激活的蛋白激酶和脑源性神经营养因子途径被激活。这些发现表明，间歇性禁食可以通过激活GSK-3β促进海马神经元的分化和成熟，从而改善学习和记忆能力。而腺苷一磷酸激活的蛋白激酶和脑源性神经营养因子途径被激活。这些发现表明，间歇性禁食可以通过激活GSK-3β促进海马神经元的分化和成熟，从而改善学习和记忆能力。
更新日期：2020-06-23
中文翻译：
间歇性禁食通过激活3xTg-AD小鼠中的GSK-3β来促进成年海马神经元分化。
适度的饮食限制可通过增加神经营养因子的表达并促进大脑中的神经发生而改善与年龄有关的慢性疾病，例如阿尔茨海默氏病（AD）。糖原合酶激酶-3β（GSK-3β）信号对于协调大脑发育过程中祖细胞的增殖和分化至关重要。GSK-3β参与饮食限制诱导的神经发生和认知改善的机制仍不清楚。六个月大的雄性3xTg-AD和野生型小鼠隔天（间歇禁食，IF）或随意（AL）喂养3个月。GSK-3β活性是通过将靶向GSK-3β的siRNA的慢病毒载体双向注入海马的齿状回区域来调节的。间歇性禁食可促进3xTg-AD小鼠的齿状回神经元分化和成熟，并改善公认的功能障碍。通过靶向GSK-3β的siRNA可以逆转这些作用。间歇性禁食后，胰岛素和蛋白激酶A信号通路被抑制，而腺苷一磷酸激活的蛋白激酶和脑源性神经营养因子通路被激活。这些发现表明，间歇性禁食可以通过激活GSK-3β促进海马神经元的分化和成熟，从而改善学习和记忆能力。而腺苷一磷酸激活的蛋白激酶和脑源性神经营养因子途径被激活。这些发现表明，间歇性禁食可以通过激活GSK-3β促进海马神经元的分化和成熟，从而改善学习和记忆能力。而腺苷一磷酸激活的蛋白激酶和脑源性神经营养因子途径被激活。这些发现表明，间歇性禁食可以通过激活GSK-3β促进海马神经元的分化和成熟，从而改善学习和记忆能力。
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