Zhu Xiongwei, Moreira Paula I, Smith Mark A, Perry George
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA.
Trends Mol Med. 2005 Sep;11(9):391-3. doi: 10.1016/j.molmed.2005.07.002.
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.
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。