Evidence map›Paper›PMID 41877246›Full record

ReviewTranslational neurodegeneration2026

Axonopathy: mechanisms and potential therapeutic targets for neurodegenerative diseases.

Ruinan Shen, Kijung Sung, Jianqing Ding, Chengbiao Wu

Abstract readReview
In one paragraph

Review in Translational neurodegeneration, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. 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

4 authors.

Ruinan ShenInstitute of Neurology, Ruijing Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Kijung SungDepartment of Neurosciences, University of California San Diego, La Jolla, San Diego, CA, USA.
Jianqing DingInstitute of Aging & Tissue Regeneration, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Chengbiao WuDepartment of Neurosciences, University of California San Diego, La Jolla, San Diego, CA, USA. chw049@health.ucsd.edu.ORCID http://orcid.org/0000-0002-3660-088X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Axons are unique structural and functional features of nerve cells, which play a critical role in regulating neuronal homeostasis. Dysfunction and degeneration of axons (axonopathy) has been established as an early and prominent contributing mechanism to the pathogenesis of neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. In this review, we briefly summarize the structure and function of axons, and highlight recent advances in the understanding of the role of axons in health and disease. We argue that axons are a potential target for developing novel therapies for neurodegenerative diseases.

Indexed as

AxonsNeurodegenerative DiseasesAnimalsHumansAlzheimer’s diseaseAmyotrophic lateral sclerosisAutophagyAxonAxonal transportHuntington’s diseaseMitochondriaNeurodegenerationNeurotrophic factorsParkinson’s disease

Identifiers

PMID41877246
PMCPMC13011709

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.