Axonal transport and Alzheimer's disease

被引:233
作者
Stokin, Gorazd B. [1 ]
Goldstein, Lawrence S. B.
机构
[1] Univ Ljubljana, Med Ctr, Div Neurophysiol, Inst Clin Neurophysiol, SI-1525 Ljubljana, Slovenia
[2] Univ Calif San Diego, Sch Med, Howard Hughes Med Inst, Dept Cellular & Mol Med, La Jolla, CA 92093 USA
关键词
motor proteins; axons; axonal pathology; aging; neurodegeneration;
D O I
10.1146/annurev.biochem.75.103004.142637
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 I 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.
引用
收藏
页码:607 / 627
页数:21
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