Abstract：
:Local axon degeneration is a common pathological feature of many neurodegenerative diseases and peripheral neuropathies. While it is believed to operate with an apoptosis-independent molecular program, the underlying molecular mechanisms are largely unknown. In this study, we used the degeneration of transected axons, termed "Wallerian degeneration," as a model to examine the possible involvement of the ubiquitin proteasome system (UPS). Inhibiting UPS activity by both pharmacological and genetic means profoundly delays axon degeneration both in vitro and in vivo. In addition, we found that the fragmentation of microtubules is the earliest detectable change in axons undergoing Wallerian degeneration, which among other degenerative events, can be delayed by proteasome inhibitors. Interestingly, similar to transected axons, degeneration of axons from nerve growth factor (NGF)-deprived sympathetic neurons could also be suppressed by proteasome inhibitors. Our findings suggest a possibility that inhibiting UPS activity may serve to retard axon degeneration in pathological conditions.
journal_name
Neuronjournal_title
Neuronauthors
Zhai Q,Wang J,Kim A,Liu Q,Watts R,Hoopfer E,Mitchison T,Luo L,He Zdoi
10.1016/s0896-6273(03)00429-xsubject
Has Abstractpub_date
2003-07-17 00:00:00pages
217-25issue
2eissn
0896-6273issn
1097-4199pii
S089662730300429Xjournal_volume
39pub_type
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