Format

Send to

Choose Destination
See comment in PubMed Commons below
Nat Rev Neurosci. 2014 Jun;15(6):394-409. doi: 10.1038/nrn3680.

Wallerian degeneration: an emerging axon death pathway linking injury and disease.

Author information

1
1] School of Biomedical Sciences, University of Nottingham, Medical School, Queen's Medical Centre, Nottingham, NG7 2UH, UK. [2].
2
1] The Babraham Institute, Babraham Research Campus, Babraham, Cambridge, CB22 3AT, UK. [2].
3
The Babraham Institute, Babraham Research Campus, Babraham, Cambridge, CB22 3AT, UK.

Abstract

Axon degeneration is a prominent early feature of most neurodegenerative disorders and can also be induced directly by nerve injury in a process known as Wallerian degeneration. The discovery of genetic mutations that delay Wallerian degeneration has provided insight into mechanisms underlying axon degeneration in disease. Rapid Wallerian degeneration requires the pro-degenerative molecules SARM1 and PHR1. Nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) is essential for axon growth and survival. Its loss from injured axons may activate Wallerian degeneration, whereas NMNAT overexpression rescues axons from degeneration. Here, we discuss the roles of these and other proposed regulators of Wallerian degeneration, new opportunities for understanding disease mechanisms and intriguing links between Wallerian degeneration, innate immunity, synaptic growth and cell death.

PMID:
24840802
DOI:
10.1038/nrn3680
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Nature Publishing Group
    Loading ...
    Support Center