Evidence map›Paper›PMID 20345246›Full record

ReviewAnnual review of neuroscience2010

Wallerian degeneration, wld(s), and nmnat.

Michael P Coleman, Marc R Freeman

Abstract readReview
In one paragraph

Review in Annual review of neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 295 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
295citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

295 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  13. FOXO1-NMNAT3 axis dysregulation promotes doxorubicin cardiotoxicity: NADRedox report : communications in free radical research · 2025
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235 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Michael P ColemanLaboratory of Molecular Signaling, The Babraham Institute, Cambridge CB223AT, United Kingdom.
Marc R Freeman

Funding

Molecular Mechanisms of Axon DegenerationR01NS059991 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI FREEMAN, MARC R · 2008 to 2023
$5.4M
Biotechnology and Biological Sciences Research CouncilNINDS NIH HHS NS059991NINDS NIH HHS R01 NS059991
6 · The paper itself

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(S)--an extraordinary protein formed by fusing a Ube4b sequence to Nmnat1--acts to protect severed axons. Interestingly, the neuroprotective effects of Wld(S) span all species tested, which suggests that there is an ancient, Wld(S)-sensitive axon destruction program. Recent studies with Wld(S) 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.

Indexed as

AnimalsAxonsAxotomyGene FusionHumansNerve Tissue ProteinsNicotinamide-Nucleotide AdenylyltransferaseUbiquitin-Protein LigasesWallerian DegenerationNerve Tissue ProteinsNicotinamide-Nucleotide AdenylyltransferaseNmnat1 protein, mouseUbe4b protein, mouseUbiquitin-Protein LigasesWld protein, mouse

Identifiers

PMID20345246
PMCPMC5223592

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.