Evidence map›Paper›PMID 38098004›Full record

ArticleImmunity & ageing : I & A2023

IL-17A promotes the progression of Alzheimer's disease in APP/PS1 mice.

Min Cao, Jing Liu, Xiaomin Zhang, Yaqi Wang, Yuli Hou, Qiao Song, Yuting Cui, Yue Zhao, Peichang Wang

Open access · goldAbstract read
In one paragraph

Article in Immunity & ageing : I & A, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.8field-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

25 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  3. Chrysin Ameliorated Neurochemical and Behavioural Changes Mediated By Combined Exposure of Interleukin-17 A With Amyloid BetaJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
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  6. Food science & nutrition · 2026
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  18. 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
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  20. Review
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

9 authors at 1 institution in 1 country.

Min Cao *Department of Clinical Laboratory, Xuanwu Hospital Capital Medical University, Beijing, 100053, People's Republic of China.
Jing Liu *Department of Clinical Laboratory, Xuanwu Hospital Capital Medical University, Beijing, 100053, People's Republic of China.
Xiaomin ZhangDepartment of Clinical Laboratory, Xuanwu Hospital Capital Medical University, Beijing, 100053, People's Republic of China.
Yaqi WangDepartment of Clinical Laboratory, Xuanwu Hospital Capital Medical University, Beijing, 100053, People's Republic of China.
Yuli HouDepartment of Clinical Laboratory, Xuanwu Hospital Capital Medical University, Beijing, 100053, People's Republic of China.
Qiao SongDepartment of Clinical Laboratory, Xuanwu Hospital Capital Medical University, Beijing, 100053, People's Republic of China.
Yuting CuiDepartment of Clinical Laboratory, Xuanwu Hospital Capital Medical University, Beijing, 100053, People's Republic of China.
Yue ZhaoDepartment of Clinical Laboratory, Xuanwu Hospital Capital Medical University, Beijing, 100053, People's Republic of China.
Peichang WangDepartment of Clinical Laboratory, Xuanwu Hospital Capital Medical University, Beijing, 100053, People's Republic of China. pcw1905@126.com.
Capital Medical University · CN

Funding

Beijing: Sail Plan for Talents Development ZYLX202114National Nature Science Foundation of China No. 81871714State Key Program of National Natural Science Foundation of China No. 82030064
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD), which is the most common cause of dementia in elderly individuals, is a progressive neurodegenerative disorder. Neuroinflammation, which is an immune response that is activated by glial cells in the central nervous system, plays an important role in neurodegenerative diseases. Many studies have shown that interleukin-17A (IL-17A) plays an important role in AD, but research on the pathological effects of IL-17A on AD is limited.

methodsWe report the effect of IL-17A on AD progression in APPswe/PS1dE9 (APP/PS1) mice, which are the most widely used AD model mice. The BV2 cell line, which is a microglial cell line derived from C57/BL6 mice, was used to establish a cell model to verify the role of IL-17A in neuroinflammation at the cellular level. The HT22 hippocampal neuronal cell line was used to investigate the relationship between IL-17A and Aβ deposition.

resultsIn this research, we found that IL-17A promotes the progression of AD in the APP/PS1 mouse model. The role of IL-17A in neuroinflammation is related to tumour necrosis factor (TNF)-α. Circulating IL-17A stimulates the secretion of TNF-α by microglia through the Toll-like receptor 4 (TLR4)/nuclear factor (NF)-κB signalling pathway, thus exacerbating neuroinflammation. In addition, intraperitoneal injection of IL-17A antibody (IL17Ab) significantly improved the cognitive function of APP/PS1 mice.

conclusionsIL-17A increased TNF-α levels in the brain and exacerbated neuroinflammation through the TLR4/NF-κB signalling pathway and microglial activation in APP/PS1 mice. Moreover, IL-17A promoted the progression of AD by enhancing neuroinflammation, inhibiting microglial phagocytosis, and promoting the deposition of β-amyloid 42 in AD model mice.

Indexed as

Alzheimer’s diseaseIL-17ANeuroinflammationTNFα

Identifiers

PMID38098004
PMCPMC10720112
OpenAlexW4389735037

What OpenQuestion holds

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Registered trials

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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.