Evidence map›Paper›PMID 39768167›Full record

ReviewCells2024

Exploring the Role of Axons in ALS from Multiple Perspectives.

Xiaosu Chen, Shuchang Lv, Jinmeng Liu, Yingjun Guan, Chunjie Xu, Xiaonan Ma, Mu Li, Xue Bai, Kexin Liu, Haoyun Zhang and 3 more

Abstract readReview
In one paragraph

Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Mechanistic study on the role of multi-pathway autophagy in ovarian aging: literature review.Apoptosis : an international journal on programmed cell death · 2025
    Review
  3. Article
  4. Review
  5. 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

13 authors.

Xiaosu ChenDepartment of Histology and Embryology, Shandong Second Medical University, Weifang 261053, China.
Shuchang LvDepartment of Histology and Embryology, Shandong Second Medical University, Weifang 261053, China.
Jinmeng LiuNeurologic Disorders and Regenerative Repair Lab of Shandong Higher Education, Shandong Second Medical University, Weifang 261053, China.ORCID 0000-0002-6041-2723
Yingjun GuanDepartment of Histology and Embryology, Shandong Second Medical University, Weifang 261053, China.
Chunjie XuDepartment of Histology and Embryology, Shandong Second Medical University, Weifang 261053, China.
Xiaonan MaDepartment of Histology and Embryology, Shandong Second Medical University, Weifang 261053, China.
Mu LiNeurologic Disorders and Regenerative Repair Lab of Shandong Higher Education, Shandong Second Medical University, Weifang 261053, China.ORCID 0000-0002-2719-8657
Xue BaiDepartment of Histology and Embryology, Shandong Second Medical University, Weifang 261053, China.
Kexin LiuNeurologic Disorders and Regenerative Repair Lab of Shandong Higher Education, Shandong Second Medical University, Weifang 261053, China.
Haoyun ZhangNeurologic Disorders and Regenerative Repair Lab of Shandong Higher Education, Shandong Second Medical University, Weifang 261053, China.
Qiupeng YanNeurologic Disorders and Regenerative Repair Lab of Shandong Higher Education, Shandong Second Medical University, Weifang 261053, China.
Fenghua ZhouNeurologic Disorders and Regenerative Repair Lab of Shandong Higher Education, Shandong Second Medical University, Weifang 261053, China.
Yanchun ChenDepartment of Histology and Embryology, Shandong Second Medical University, Weifang 261053, China.ORCID 0009-0007-7777-138X

Funding

Shandong Province Natural Science Foundation of China ZR2024MH112; ZR2024QH628The National Natural Science Foundation of China 82271483Weifang Science and Technology Development Plan Project 2023YX036; 2022YX043
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS), commonly known as motor neuron disease, is a neurodegenerative disorder characterized by the progressive degeneration of both upper and lower motor neurons. This pathological process results in muscle weakness and can culminate in paralysis. To date, the precise etiology of ALS remains unclear. However, a burgeoning body of research indicates that axonal dysfunction is a pivotal element in the pathogenesis of ALS and significantly influences the progression of disease. Dysfunction of axons in ALS can result in impediments to nerve impulse transmission, leading to motor impairment, muscle atrophy, and other associated complications that severely compromise patients' quality of life and survival prognosis. In this review, we concentrate on several key areas: the ultrastructure of axons, the mechanisms of axonal degeneration in ALS, the impact of impaired axonal transport on disease progression in ALS, and the potential for axonal regeneration within the central nervous system (CNS). Our objective is to achieve a more holistic and profound understanding of the multifaceted role that axons play in ALS, thereby offering a more intricate and refined perspective on targeted axonal therapeutic interventions.

Indexed as

Amyotrophic Lateral SclerosisAxonsAnimalsAxonal TransportDisease ProgressionHumansMotor Neuronsamyotrophic lateral sclerosisaxon degenerationaxon regenerationaxon transporttherapy

Identifiers

PMID39768167
PMCPMC11674045

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.