Evidence map›Paper›PMID 31071521›Full record

ReviewCurrent opinion in neurobiology2019

Mechanisms of injury-induced axon degeneration.

Chen Ding, Marc Hammarlund

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Redox Molecules in Aging and Neurodegenerative Disorders.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Loss of SARM1 ameliorates secondary thalamic neurodegeneration after cerebral infarction.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article
  7. Article
  8. Autonomic Modulation of Atrial Fibrillation.JACC. Basic to translational science · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. SARM1 can be a potential therapeutic target for spinal cord injury.Cellular and molecular life sciences : CMLS · 2022
    Review
  15. In Vivo Molecular Changes in the Retina of Patients With Multiple Sclerosis.Investigative ophthalmology & visual science · 2021
    Article
  16. Article
  17. Article
  18. Degeneration of Injured Axons and Dendrites Requires Restraint of a Protective JNK Signaling Pathway by the Transmembrane Protein Raw.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  19. Editorial overview: Molecular neuroscience.Current opinion in neurobiology · 2019
    Article
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 at 1 institution in 1 country.

Chen DingDepartment of Neuroscience, Yale University, New Haven, United States.
Marc HammarlundDepartment of Neuroscience, Yale University, New Haven, United States; Department of Genetics, Yale University, New Haven, United States. Electronic address: marc.hammarlund@yale.edu.
Yale University · US

Funding

Discovery and analysis of the C. elegans neuronal gene expression network (CENGEN)R01NS100547 · NINDS · YALE UNIVERSITY · PI MARC HAMMARLUND, Oliver Hobert · 2017 to 2026
$11.2M
New Mechanisms in Axon RegenerationR01NS094219 · NINDS · YALE UNIVERSITY · PI HAMMARLUND, MARC · 2015 to 2025
$4.0M
Evaluation of Novel Axon Regeneration Targets for Spinal Cord injury TherapyR01NS098817 · NINDS · YALE UNIVERSITY · PI HAMMARLUND, MARC, STRITTMATTER, STEPHEN M · 2016 to 2020
$1.4M
NINDS NIH HHS R01 NS094219NINDS NIH HHS R01 NS098817NINDS NIH HHS R01 NS100547
6 · The paper itself

Abstract

Injury-induced axon degeneration in model organisms and cell culture has emerged as an area of growing interest due to its experimental tractability and to the promise of identifying conserved mechanisms that mediate axon loss in human disease. Injury-induced axon degeneration is also observed within the well-studied process of Wallerian degeneration, a complex phenomenon triggered by axon injury to peripheral nerves in mammals. Recent studies have led to the identification of key molecular components of injury-induced axon degeneration. Axon survival factors, such as NMNAT2, act to protect injured axons from degeneration. By contrast, factors such as SARM1, MAPK, and PHR1 act to promote degeneration. The coordinated activity of these factors determines axon fate after injury. Since axon loss is an early feature of neurodegenerative diseases, it is possible that understanding the molecular mechanism of injury-induced degeneration will lead to new treatments for axon loss in neurodegenerative disease. Here, we discuss the critical pathways for injury-induced axon degeneration across species with an emphasis on their interactions in an integrated signaling network.

Indexed as

AxonsNeurodegenerative DiseasesAnimalsHumansNicotinamide-Nucleotide AdenylyltransferaseSignal TransductionWallerian DegenerationNicotinamide-Nucleotide Adenylyltransferase

Identifiers

PMID31071521
PMCPMC6629473
OpenAlexW2944541145

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.