Polyglutamines stop traffic: Axonal transport as a common target in neurodegenerative diseases

被引:24
作者
Feany, MB
La Spada, AR
机构
[1] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Neuropathol,Dept Pathol, Boston, MA 02115 USA
[2] Univ Washington, Med Ctr, Dept Lab Med, Div Med Genet,Div Neurogenet, Seattle, WA 98195 USA
关键词
D O I
10.1016/S0896-6273(03)00600-7
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
In this issue of Neuron, two papers provide evidence that polyglutamine (polyQ) proteins disrupt axonal transport. Gunawardena et al. show that normal levels of huntingtin are required for proper axonal transport in Drosophila. In addition, expression of expanded polyQ proteins disrupts axonal transport in larval neurons. Szebenyi and colleagues find that polyQ proteins directly inhibit fast axonal transport using axoplasm from the squid giant axon and suggest that axonal transport defects may be a common feature of polyQ disease pathogenesis.
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页码:1 / 2
页数:2
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