Evidence map›Paper›PMID 36823558›Full record

ArticleBMC neuroscience2023

Activation of the IL-17/TRAF6/NF-κB pathway is implicated in Aβ-induced neurotoxicity.

Yulan Liu, Yang Meng, Chenliang Zhou, Juanjuan Yan, Cuiping Guo, Weiguo Dong

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Trichomonas vaginalis-induced inflammation is associated with Th17 differentiation and tumor-intrinsic IL-17R signaling in prostate cancer progression.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. IL-17 A Exacerbated Neuroinflammatory and Neurodegenerative Biomarkers in Intranasal Amyloid-Beta Model of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Yulan Liu *Department of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, China.
Yang Meng *Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Chenliang ZhouDepartment of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, China.
Juanjuan YanDepartment of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, China.
Cuiping GuoDepartment of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, China. rm003778@whu.edu.cn.
Weiguo DongDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, China. dongweiguo@whu.edu.cn.
Renmin Hospital of Wuhan University · CNWuhan University · CN

Funding

National Natural Science Foundation of China 8187032070the Fundamental Research Funds for the Central Universities 2042019kf0081
6 · The paper itself

Abstract

backgroundNeuroinflammation plays a critical role in Amyloid-β (Aβ) pathophysiology. The cytokine, interleukin-17A (IL-17) is involved in the learning and memory process in the central nervous system and its level was reported to be increased in Alzheimer's disease (AD) brain, while the effect of IL-17 on the course of Aβ has not been well defined.

methodsHere, we used APP/PS1 mice to detect the IL-17 expression level. Primary hippocampal neurons were treated with IL-17, and immunofluorescence was used to investigate whether IL-17 induced neuron damage. At the same time, male C57BL/6 mice were injected with Aβ

resultsAltogether, we here found that IL-17 was increased in APP/PS1 mice, and it induced neural damage by the administration to primary hippocampal neurons. Interestingly, Using Aβ

conclusionThese findings highlight the pathogenic role of IL-17 in Aβ induced-synaptic dysfunction and cognitive deficits. Inhibition of IL-17 could ameliorate Aβ-induced neurotoxicity and cognitive decline in C57BL/6 mice by downregulation of the TRAF6/NF-κB pathway, which provides new clues for the mechanism of Aβ-induced cognitive impairments, and a basis for therapeutic intervention.

Indexed as

Alzheimer DiseaseCognitive DysfunctionAmyloid beta-PeptidesAnimalsDisease Models, AnimalInterleukin-17MaleMiceMice, Inbred C57BLMice, TransgenicNF-kappa BTNF Receptor-Associated Factor 6Amyloid beta-PeptidesInterleukin-17NF-kappa BTNF Receptor-Associated Factor 6Amyloid-βCognitive declineIL-17IL-17AbSynaptic dysfunction

Identifiers

PMID36823558
PMCPMC9951515
OpenAlexW4321614664

What OpenQuestion 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 OpenQuestion graph.