Evidence map›Paper›PMID 26844829›Full record

ReviewNeuron2016

Axon Self-Destruction: New Links among SARM1, MAPKs, and NAD+ Metabolism.

Josiah Gerdts, Daniel W Summers, Jeffrey Milbrandt, Aaron DiAntonio

Open access · bronzeAbstract readReview
In one paragraph

Review in Neuron, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 204 papers.

0numbers the graph read from it
0cells of the map it votes in
204citing papers in PubMed
23.7field-weighted citation impact, top 1% of its field
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

204 citing papers in PubMed, 332 citations in OpenAlex.

  1. Peripheral Neuropathy in Metabolic Stress.International journal of molecular sciences · 2026
    Review
  2. Review
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  5. Hyperglycemia promotes SIRT3-mediated deacetylation of SARM1 to exacerbate diabetic peripheral neuropathy in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Article
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  8. IL1A enhances TNF-induced retinal ganglion cell death.Frontiers in aging neuroscience · 2026
    Article
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  14. Review
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144 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

4 authors at 1 institution in 1 country.

Josiah GerdtsDepartment of Genetics, Washington University School of Medicine in St. Louis, 660 Euclid Avenue, St. Louis, MO 63110, USA.
Daniel W SummersDepartment of Genetics, Washington University School of Medicine in St. Louis, 660 Euclid Avenue, St. Louis, MO 63110, USA; Department of Developmental Biology, Washington University School of Medicine in St. Louis, 660 Euclid Avenue, St. Louis, MO 63110, USA.
Jeffrey MilbrandtDepartment of Genetics, Washington University School of Medicine in St. Louis, 660 Euclid Avenue, St. Louis, MO 63110, USA; Hope Center for Neurological Disorders, Washington University School of Medicine in St. Louis, 660 Euclid Avenue, St. Louis, MO 63110, USA.
Aaron DiAntonioDepartment of Developmental Biology, Washington University School of Medicine in St. Louis, 660 Euclid Avenue, St. Louis, MO 63110, USA; Hope Center for Neurological Disorders, Washington University School of Medicine in St. Louis, 660 Euclid Avenue, St. Louis, MO 63110, USA. Electronic address: diantonio@wustl.edu.
Washington University in St. Louis · US

Funding

PHYSIOLOGY AND GENETICS OF THE GDNF HOMOLOG NEURTURINR01AG013730 · NIA · WASHINGTON UNIVERSITY · PI JEFFREY D MILBRANDT · 1996 to 2026
$10.6M
DISSECTION OF SARM1-INDUCED AXON DEGENERATION AND CELL DEATHR01NS087632 · NINDS · WASHINGTON UNIVERSITY · PI Aaron Diantonio, JEFFREY D MILBRANDT · 2014 to 2026
$6.4M
Regulation of axonal degeneration by the DLK kinaseR37NS065053 · NINDS · WASHINGTON UNIVERSITY · PI Aaron Diantonio · 2020 to 2026
$4.3M
MOLECULAR PATHWAYS REGULATING SYNAPTIC GROWTHR01DA020812 · NIDA · WASHINGTON UNIVERSITY · PI DIANTONIO, AARON · 2007 to 2016
$3.3M
REGULATION OF AXONAL DEGENERATION BY THE DLK KINASER01NS065053 · NINDS · WASHINGTON UNIVERSITY · PI DIANTONIO, AARON · 2010 to 2019
$3.3M
NIA NIH HHS R01 AG013730NIDA NIH HHS DA020812NIDA NIH HHS R01 DA020812NINDS NIH HHS NS065053NINDS NIH HHS NS087632NINDS NIH HHS R01 NS065053NINDS NIH HHS R01 NS087632NINDS NIH HHS R37 NS065053
6 · The paper itself

Abstract

Wallerian axon degeneration is a form of programmed subcellular death that promotes axon breakdown in disease and injury. Active degeneration requires SARM1 and MAP kinases, including DLK, while the NAD+ synthetic enzyme NMNAT2 prevents degeneration. New studies reveal that these pathways cooperate in a locally mediated axon destruction program, with NAD+ metabolism playing a central role. Here, we review the biology of Wallerian-type axon degeneration and discuss the most recent findings, with special emphasis on critical signaling events and their potential as therapeutic targets for axonopathy.

Indexed as

Signal TransductionAnimalsArmadillo Domain ProteinsAxonsCytoskeletal ProteinsHumansMitogen-Activated Protein KinasesNADNeuroprotective AgentsNicotinamide-Nucleotide AdenylyltransferaseWallerian DegenerationArmadillo Domain ProteinsCytoskeletal ProteinsMitogen-Activated Protein KinasesNADNeuroprotective AgentsNicotinamide-Nucleotide AdenylyltransferaseNmnat2 protein, mouseSARM1 protein, mouse

Identifiers

PMID26844829
PMCPMC4742785
OpenAlexW2257942016

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.