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轴突运输与阿尔茨海默病

Axonal transport and Alzheimer's disease.

作者信息

Stokin Gorazd B, Goldstein Lawrence S B

机构信息

Institute of Clinical Neurophysiology, Division of Neurology, University Medical Center, SI-1525 Ljubljana, Slovenia.

出版信息

Annu Rev Biochem. 2006;75:607-27. doi: 10.1146/annurev.biochem.75.103004.142637.

Abstract

In contrast to most eukaryotic cells, neurons possess long, highly branched processes called axons and dendrites. In large mammals, such as humans, some axons reach lengths of over 1 m. These lengths pose a major challenge to the movement of proteins, vesicles, and organelles between presynaptic sites and cell bodies. To overcome this challenge axons and dendrites rely upon specialized transport machinery consisting of cytoskeletal motor proteins generating directed movements along cytoskeletal tracks. Not only are these transport systems crucial to maintain neuronal viability and differentiation, but considerable experimental evidence suggests that failure of axonal transport may play a role in the development or progression of neurological diseases such as Alzheimer's disease.

摘要

与大多数真核细胞不同,神经元具有称为轴突和树突的长且高度分支的突起。在大型哺乳动物(如人类)中,一些轴突的长度超过1米。这些长度对蛋白质、囊泡和细胞器在突触前位点与细胞体之间的移动构成了重大挑战。为了克服这一挑战,轴突和树突依赖于由细胞骨架运动蛋白组成的特殊运输机制,这些蛋白沿着细胞骨架轨道产生定向运动。这些运输系统不仅对于维持神经元的活力和分化至关重要,而且大量实验证据表明轴突运输的失败可能在诸如阿尔茨海默病等神经疾病的发生或发展中起作用。

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