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J Cell Biol. 2012 Jan 9;196(1):7-18. doi: 10.1083/jcb.201108111.

Axon degeneration: molecular mechanisms of a self-destruction pathway.

Author information

1
Department of Neurobiology, Stanford University School of Medicine, Stanford, CA 94305, USA. jtw@stanford.edu

Abstract

Axon degeneration is a characteristic event in many neurodegenerative conditions including stroke, glaucoma, and motor neuropathies. However, the molecular pathways that regulate this process remain unclear. Axon loss in chronic neurodegenerative diseases share many morphological features with those in acute injuries, and expression of the Wallerian degeneration slow (WldS) transgene delays nerve degeneration in both events, indicating a common mechanism of axonal self-destruction in traumatic injuries and degenerative diseases. A proposed model of axon degeneration is that nerve insults lead to impaired delivery or expression of a local axonal survival factor, which results in increased intra-axonal calcium levels and calcium-dependent cytoskeletal breakdown.

PMID:
22232700
PMCID:
PMC3255986
DOI:
10.1083/jcb.201108111
[Indexed for MEDLINE]
Free PMC Article

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