Wallerian degeneration, WldS, and Nmnat

Michael P. Coleman, Marc Freeman

Research output: Contribution to journalReview article

282 Citations (Scopus)

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 Wld San extraordinary protein formed by fusing a Ube4b sequence to Nmnat1acts 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.

Original languageEnglish (US)
Pages (from-to)245-267
Number of pages23
JournalAnnual Review of Neuroscience
Volume33
DOIs
StatePublished - 2010
Externally publishedYes

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Wallerian Degeneration
Axons
Axotomy
Neuroprotective Agents
Research Personnel

Keywords

  • axon
  • axonal transport
  • dying back disorder
  • Wallerian-like degeneration

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Wallerian degeneration, WldS, and Nmnat. / Coleman, Michael P.; Freeman, Marc.

In: Annual Review of Neuroscience, Vol. 33, 2010, p. 245-267.

Research output: Contribution to journalReview article

Coleman, Michael P. ; Freeman, Marc. / Wallerian degeneration, WldS, and Nmnat. In: Annual Review of Neuroscience. 2010 ; Vol. 33. pp. 245-267.
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