Evidence map›Paper›PMID 38727249›Full record

ReviewCNS neuroscience & therapeutics2024

Current evidence of synaptic dysfunction after stroke: Cellular and molecular mechanisms.

Chuan Li, Min Jiang, Zhi-Ting Fang, Zhiying Chen, Li Li, Ziying Liu, Junmin Wang, Xiaoping Yin, Jian Wang, Moxin Wu

Abstract readReview
In one paragraph

Review in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
–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

26 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  13. Neuromodulation and cognition in late-life depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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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

10 authors.

Chuan LiDepartment of Medical Laboratory, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi, China.
Min JiangJiujiang Clinical Precision Medicine Research Center, Jiujiang, Jiangxi, China.
Zhi-Ting FangDepartment of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Zhiying ChenDepartment of Neurology, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi, China.
Li LiDepartment of Intensive Care Unit, The Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi, China.
Ziying LiuDepartment of Medical Laboratory, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi, China.
Junmin WangDepartment of Human Anatomy, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Xiaoping YinDepartment of Neurology, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi, China.
Jian WangDepartment of Human Anatomy, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China.ORCID 0000-0003-2291-640X
Moxin WuDepartment of Medical Laboratory, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi, China.

Funding

Education Department of Jiangxi Province GJJ201834Jiangxi Provincial Health Commission Science and Technology Plan project 202212021National Natural Science Foundation of China 81960221National Natural Science Foundation of China 82260209National Natural Science Foundation of China 82371339Natural Science Foundation of Jiangxi Province 20232BAB206046
6 · The paper itself

Abstract

backgroundStroke is an acute cerebrovascular disease in which brain tissue is damaged due to sudden obstruction of blood flow to the brain or the rupture of blood vessels in the brain, which can prompt ischemic or hemorrhagic stroke. After stroke onset, ischemia, hypoxia, infiltration of blood components into the brain parenchyma, and lysed cell fragments, among other factors, invariably increase blood-brain barrier (BBB) permeability, the inflammatory response, and brain edema. These changes lead to neuronal cell death and synaptic dysfunction, the latter of which poses a significant challenge to stroke treatment.

resultsSynaptic dysfunction occurs in various ways after stroke and includes the following: damage to neuronal structures, accumulation of pathologic proteins in the cell body, decreased fluidity and release of synaptic vesicles, disruption of mitochondrial transport in synapses, activation of synaptic phagocytosis by microglia/macrophages and astrocytes, and a reduction in synapse formation.

conclusionsThis review summarizes the cellular and molecular mechanisms related to synapses and the protective effects of drugs or compounds and rehabilitation therapy on synapses in stroke according to recent research. Such an exploration will help to elucidate the relationship between stroke and synaptic damage and provide new insights into protecting synapses and restoring neurologic function.

Indexed as

StrokeSynapsesAnimalsHumansastrocytesmicrogliastrokesynapse pruningsynaptic dysfunction

Identifiers

PMID38727249
PMCPMC11084978

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.