|国家预印本平台
首页|阿尔茨海默病神经元细胞周期再进入的研究进展

阿尔茨海默病神经元细胞周期再进入的研究进展

Research progress about re-entering cell cycle of neurons in Alzheimer's disease

中文摘要英文摘要

背景:目前阿尔茨海默病(Alzheimer's Disease, AD)的病理机制学说有Aβ沉积、Tau蛋白磷酸化异常、氧化应激、炎症等假说,但以上任何一种假说都不能解释AD的全部病理特征。研究现状:"神经退行性变--细胞周期"假说打破了过去一直认为"神经元处于一种有丝分裂后的终末分化状态"的理论,提出在神经退行性变等病理情况下,神经元可进行分裂增殖,重新进入细胞周期,但这些被迫重新进入细胞周期后的神经元并不能继续分化,而是走向死亡。AD中受损神经元重新进入细胞周期已证实为AD早期主要病理特征之一,细胞周期调控异常被证实与AD的所有病理特征相关联,且该特征的出现要早于神经原纤维缠结与老年斑,并持续整个AD病程。研究用途:"神经退行性变-细胞周期"假说对于阐述AD病理机制、AD诊断及治疗均有非常重要的意义。

Backgrounds: At present, hypotheses of pathological mechanism of Alzheimer's disease(AD) include A β deposition, abnormal Tau protein phosphorylation, oxidative stress and inflammation. But none of above hypotheses can explain all the pathological features of AD. Current Status: "Neurodegeneration-cell cycle" hypothesis has broken the past theory of "neurons were in a state of terminal differentiation after mitotic division", which puts forward that neurons may proliferate and re-enter cell cycle in neurodegeneration and other pathological conditions. But neurons forced back into cell cycle of could not continue to differentiate, but to death. Re-entering cell cycle of damaged neurons in AD has been confirmed to be one of earliest pathological features of AD. Cell cycle regulation abnormality, which appears earlier than neurofibrillary tangles and senile plaques, may be associated with all pathologic features of AD and continues throughout the course of AD. Research Purposes: "Neurodegeneration-cell cycle" hypothesis might contribute to explain pathological mechanism, diagnosis and therapy of AD.

周小英、高旭光

神经病学、精神病学基础医学细胞生物学

阿尔茨海默病细胞周期检验点

lzheimer's diseaseCell CycleCheckpoint

周小英,高旭光.阿尔茨海默病神经元细胞周期再进入的研究进展[EB/OL].(2013-11-21)[2025-08-02].http://www.paper.edu.cn/releasepaper/content/201311-419.点此复制

评论