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阿尔茨海默病:一种细胞内运动障碍?

Alzheimer's disease: an intracellular movement disorder?

作者信息

Zhu Xiongwei, Moreira Paula I, Smith Mark A, Perry George

机构信息

Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA.

出版信息

Trends Mol Med. 2005 Sep;11(9):391-3. doi: 10.1016/j.molmed.2005.07.002.

Abstract

Axonal transport is essential for maintaining the structure and function of nerve cells. Deficient axonal transport has been implicated in several neurodegenerative diseases, including Alzheimer's disease (AD). In addition to a disturbed cytoskeleton and other abnormalities observed in AD that are suggestive of axonal transport deficits, several AD-related proteins are implicated in the regulation of axonal transport. A recent study has demonstrated that the axonal transport deficit occurs early in the course of AD, preceding amyloid pathology substantially in mouse models of AD; more importantly, the study showed that reduced axonal transport leads to increased amyloid beta production and deposition. These data place axonal transport deficits at a central point in the pathogenesis of AD.

摘要

轴突运输对于维持神经细胞的结构和功能至关重要。轴突运输缺陷与包括阿尔茨海默病(AD)在内的几种神经退行性疾病有关。除了在AD中观察到的提示轴突运输缺陷的细胞骨架紊乱和其他异常外,几种与AD相关的蛋白质也参与轴突运输的调节。最近一项研究表明,在AD病程早期就出现轴突运输缺陷,在AD小鼠模型中,该缺陷大大早于淀粉样蛋白病理改变;更重要的是,该研究表明轴突运输减少会导致β淀粉样蛋白生成和沉积增加。这些数据表明轴突运输缺陷在AD发病机制中处于核心地位。

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