Evidence map›Paper›PMID 25617478›Full record

ReviewNeuroscience letters2015

Mechanisms of distal axonal degeneration in peripheral neuropathies.

Christopher R Cashman, Ahmet Höke

Abstract readReview
In one paragraph

Review in Neuroscience letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 1 pooled it
12.5field-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

123 citing papers in PubMed, 1 synthesis or guideline pooled it, 191 citations in OpenAlex.

  1. Pooled it
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  15. Diabetic neuropathy: cutting-edge research and future directions.Signal transduction and targeted therapy · 2025
    Review
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  17. The relevance of combined testing of cerebrospinal fluid glial fibrillary acidic protein and ubiquitin C-terminal hydrolase L1 in multiple sclerosis and peripheral neuropathy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
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63 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 at 2 institutions in 1 country.

Christopher R CashmanDepartments of Neuroscience and Neurology, USA; MSTP- MD/PhD Program, Johns Hopkins University, Baltimore, MD 21205, USA.
Ahmet HökeDepartments of Neuroscience and Neurology, USA. Electronic address: ahoke@jhmi.edu.
Johns Hopkins University · USNeurosciences Institute · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007309 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI COX, ANDREA L · 1985 to 2019
$43.2M
HIV and antiretroviral toxic neuropathyR01NS043991 · NINDS · JOHNS HOPKINS UNIVERSITY · PI HOKE, AHMET · 2002 to 2011
$3.4M
NIGMS NIH HHS T32 GM007309NINDS NIH HHS R01 NS043991NINDS NIH HHS R01 NS-43991
6 · The paper itself

Abstract

Peripheral neuropathy is a common complication of a variety of diseases and treatments, including diabetes, cancer chemotherapy, and infectious causes (HIV, hepatitis C, and Campylobacter jejuni). Despite the fundamental difference between these insults, peripheral neuropathy develops as a combination of just six primary mechanisms: altered metabolism, covalent modification, altered organelle function and reactive oxygen species formation, altered intracellular and inflammatory signaling, slowed axonal transport, and altered ion channel dynamics and expression. All of these pathways converge to lead to axon dysfunction and symptoms of neuropathy. The detailed mechanisms of axon degeneration itself have begun to be elucidated with studies of animal models with altered degeneration kinetics, including the slowed Wallerian degeneration (Wld(S)) and Sarm knockout animal models. These studies have shown axonal degeneration to occur through a programmed pathway of injury signaling and cytoskeletal degradation. Insights into the common disease insults that converge on the axonal degeneration pathway promise to facilitate the development of therapeutics that may be effective against other mechanisms of neurodegeneration.

Indexed as

Axonal TransportCampylobacter jejuniDiabetic NeuropathiesEndoplasmic ReticulumHepacivirusHIVHumansInflammationIon ChannelsMitochondriaOrganellesPeripheral Nervous System DiseasesReactive Oxygen SpeciesSignal TransductionIon ChannelsReactive Oxygen SpeciesCampylobacter jejuniChemotherapy induced peripheral neuropathyDiabetesGuillain–Barré syndromeHIV neuropathyMechanisms of neuropathyMitochondrial agingPeripheral neuropathyPost-infectious neuropathyWld(S)

Identifiers

PMID25617478
PMCPMC4428955
OpenAlexW1966613216

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.