1932

Abstract

Traditionally, researchers have believed that axons are highly dependent on their cell bodies for long-term survival. However, recent studies point to the existence of axon-autonomous mechanism(s) that regulate rapid axon degeneration after axotomy. Here, we review the cellular and molecular events that underlie this process, termed Wallerian degeneration. We describe the biphasic nature of axon degeneration after axotomy and our current understanding of how WldS—an extraordinary protein formed by fusing a Ube4b sequence to Nmnat1—acts to protect severed axons. Interestingly, the neuroprotective effects of WldS span all species tested, which suggests that there is an ancient, WldS-sensitive axon destruction program. Recent studies with WldS also reveal that Wallerian degeneration is genetically related to several dying back axonopathies, thus arguing that Wallerian degeneration can serve as a useful model to understand, and potentially treat, axon degeneration in diverse traumatic or disease contexts.

Loading

Article metrics loading...

/content/journals/10.1146/annurev-neuro-060909-153248
2010-07-21
2024-03-28
Loading full text...

Full text loading...

/content/journals/10.1146/annurev-neuro-060909-153248
Loading
/content/journals/10.1146/annurev-neuro-060909-153248
Loading

Data & Media loading...

  • Article Type: Review Article
This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error