Evidence map›Paper›PMID 37978517›Full record

ArticleImmunity & ageing : I & A2023

Exercise improves cognitive dysfunction and neuroinflammation in mice through Histone H3 lactylation in microglia.

Hao Han, Yawei Zhao, Junda Du, Sushan Wang, Xuehan Yang, Weijie Li, Jiayi Song, Siwei Zhang, Ziyi Zhang, Yongfei Tan and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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 70 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 2 pooled it
9.1field-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

70 citing papers in PubMed, 2 syntheses or guidelines pooled it, 74 citations in OpenAlex.

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10 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

13 authors at 5 institutions in 2 countries.

Hao Han *Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Yawei Zhao *Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Junda DuSchool of Pharmaceutical Sciences, Jilin University, Changchun, 130021, China.
Sushan WangKey Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Xuehan YangKey Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Weijie LiKey Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Jiayi SongKey Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Siwei ZhangKey Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China.
Ziyi ZhangThe Second Hospital of Jilin University, Changchun, 130041, China.
Yongfei TanSouth China Institute of Collaborative Innovation, Dongguan, 523808, China.
Grant M HatchDepartments of Pharmacology and Therapeutics, Biochemistry and Medical Genetics, Center for Research and Treatment of Atherosclerosis, DREAM Children's Hospital Research Institute of Manitoba, University of Manitoba, Winnipeg, MB, R3E0T6, Canada.
Ming ZhangKey Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China. zhangming99@jlu.edu.cn.
Li ChenKey Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, 130021, China. chenl@jlu.edu.cn.
Jilin University · CNJilin Medical University · CNChildren's Hospital Research Institute of Manitoba · CASecond Affiliated Hospital of Jilin University · CNSouth China Institute of Collaborative Innovation · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExercise is postulated to be a promising non-pharmacological intervention for the improvement of neurodegenerative disease pathology. However, the mechanism of beneficial effects of exercise on the brain remains to be further explored. In this study, we investigated the effect of an exercise-induced metabolite, lactate, on the microglia phenotype and its association with learning and memory.

resultsMicroglia were hyperactivated in the brains of AlCl

conclusionThe elevated lactate acted as an "accelerator" of the endogenous "lactate timer" in microglia promoting this transition of microglia polarization balance through lactylation. These findings demonstrate that exercise-induced lactate accelerates the phenotypic transition of microglia, which plays a key role in reducing neuroinflammation and improving cognitive function.

Indexed as

Alzheimers diseaseExerciseLactateLactylationMicrogliaNeuroinflammation

Identifiers

PMID37978517
PMCPMC10655345
OpenAlexW4388770617

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.