Evidence map›Paper›PMID 37433768›Full record

ReviewSignal transduction and targeted therapy2023

Role of neuroinflammation in neurodegeneration development.

Weifeng Zhang, Dan Xiao, Qinwen Mao, Haibin Xia

Open access · goldAbstract readReview
In one paragraph

Review in Signal transduction and targeted therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 949 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
949citing papers in PubMed, 4 pooled it
226.4field-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

949 citing papers in PubMed, 4 syntheses or guidelines pooled it, 1,284 citations in OpenAlex.

  1. Pooled it
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  5. Article
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  8. The microbiota-proteostasis axis: implications in neurodegenerative diseases.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Review
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  19. Role of HMGB1 in Neuroinflammation.Molecular neurobiology · 2026
    Review
  20. Review

889 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 3 institutions in 2 countries.

Weifeng Zhang *Laboratory of Gene Therapy, Department of Biochemistry, College of Life Sciences, Shaanxi Normal University, 199 South Chang'an Road, Xi'an, 710062, P.R. China.ORCID 0000-0002-6176-4907
Dan Xiao *The State Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, Air Force Medical University, No. 169 Changle West Road, Xi'an, 710032, P.R. China.
Qinwen MaoDepartment of Pathology, University of Utah, Huntsman Cancer Institute, 2000 Circle of Hope Drive, Salt Lake City, UT, 84112, USA.
Haibin XiaLaboratory of Gene Therapy, Department of Biochemistry, College of Life Sciences, Shaanxi Normal University, 199 South Chang'an Road, Xi'an, 710062, P.R. China. hbxia2001@163.com.ORCID 0000-0002-2038-5759
Shaanxi Normal University · CNUniversity of Utah · USXijing Hospital · CN

Funding

Utah Center for Clinical and Translational ScienceUL1TR002538 · NCATS · UNIVERSITY OF UTAH · PI HESS, RACHEL, MAJERSIK, JENNIFER JUHL · 2018 to 2022
$26.0M
NCATS NIH HHS UL1 TR002538
6 · The paper itself

Abstract

Studies in neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease and Amyotrophic lateral sclerosis, Huntington's disease, and so on, have suggested that inflammation is not only a result of neurodegeneration but also a crucial player in this process. Protein aggregates which are very common pathological phenomenon in neurodegeneration can induce neuroinflammation which further aggravates protein aggregation and neurodegeneration. Actually, inflammation even happens earlier than protein aggregation. Neuroinflammation induced by genetic variations in CNS cells or by peripheral immune cells may induce protein deposition in some susceptible population. Numerous signaling pathways and a range of CNS cells have been suggested to be involved in the pathogenesis of neurodegeneration, although they are still far from being completely understood. Due to the limited success of traditional treatment methods, blocking or enhancing inflammatory signaling pathways involved in neurodegeneration are considered to be promising strategies for the therapy of neurodegenerative diseases, and many of them have got exciting results in animal models or clinical trials. Some of them, although very few, have been approved by FDA for clinical usage. Here we comprehensively review the factors affecting neuroinflammation and the major inflammatory signaling pathways involved in the pathogenicity of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and Amyotrophic lateral sclerosis. We also summarize the current strategies, both in animal models and in the clinic, for the treatment of neurodegenerative diseases.

Indexed as

Alzheimer DiseaseAmyotrophic Lateral SclerosisParkinson DiseaseAnimalsClinical Trials as TopicDisease Models, AnimalHumansInflammationNeuroinflammatory DiseasesProtein AggregatesProtein Aggregates

Identifiers

PMID37433768
PMCPMC10336149
OpenAlexW4383894096

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.