Dietary regulation of PI3K/AKT/GSK-3β pathway in Alzheimer's disease.

Dietary regulation of PI3K/AKT/GSK-3β pathway in Alzheimer's disease.
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DOI:
10.1186/alzrt265
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发表时间:
2014
期刊:
Alzheimer's research & therapy
影响因子:
--
通讯作者:
Matsuda S
Matsuda S
中科院分区:
其他
文献类型:
--
作者:
Kitagishi Y;Nakanishi A;Ogura Y;Matsuda S

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阿尔茨海默病(AD)的特征在于老年斑和由磷酸化Tau组成的神经元缠结的形成。一些发现表明,纠正AD中Tau磷酸化的信号失调可能提供一种潜在的治疗方法。PI 3 K/AKT/GSK-3β通路在神经保护中发挥关键作用,通过刺激细胞增殖和抑制细胞凋亡来增强细胞存活。该途径似乎在AD中至关重要,因为它促进Tau中的蛋白质过度磷酸化。了解这些规则可以提供新的治疗方法的更好的效果。本文就PI 3 K/AKT/GSK-3β信号通路在神经细胞信号转导中的研究进展作一综述。我们还回顾了最近的研究特点的几种饮食和信号通路参与AD。
Alzheimer’s disease (AD) is characterized by the formation of senile plaques and neurofibrillary tangles composed of phosphorylated Tau. Several findings suggest that correcting signal dysregulation for Tau phosphorylation in AD may offer a potential therapeutic approach. The PI3K/AKT/GSK-3β pathway has been shown to play a pivotal role in neuroprotection, enhancing cell survival by stimulating cell proliferation and inhibiting apoptosis. This pathway appears to be crucial in AD because it promotes protein hyper-phosphorylation in Tau. Understanding those regulations may provide a better efficacy of new therapeutic approaches. In this review, we summarize advances in the involvement of the PI3K/AKT/GSK-3β pathways in cell signaling of neuronal cells. We also review recent studies on the features of several diets and the signaling pathway involved in AD.
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