Evidence map›Paper›PMID 37084025›Full record

ArticleJournal of molecular neuroscience : MN2023

GM1 Reduced the Symptoms of Autism Spectrum Disorder by Suppressing α-Syn Through Activating Autophagy.

Baoqi Yin, Honglei Li, Pengju Zhao, Yonghong Zhao, Ruijuan Zheng, Pengya Feng, Cuixiang Xu, Enyao Li, Liguo Li

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular neuroscience : MN, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Sphingolipids in Emotional Well-Being.Journal of neurochemistry · 2026
    Review
  2. Review
  3. Umbelliprenin via increase in theFrontiers in pharmacology · 2023
    Article
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 2 institutions in 1 country.

Baoqi Yin *Department of Children Rehabilitation, The Fifth Affiliated Hospital of Zhengzhou University, No.3 Rehabilitation Street, Zhengzhou, 450052, People's Republic of China.
Honglei Li *Department of Children Rehabilitation, The Fifth Affiliated Hospital of Zhengzhou University, No.3 Rehabilitation Street, Zhengzhou, 450052, People's Republic of China.
Pengju ZhaoDepartment of Children Rehabilitation, The Fifth Affiliated Hospital of Zhengzhou University, No.3 Rehabilitation Street, Zhengzhou, 450052, People's Republic of China.
Yonghong ZhaoDepartment of Children Rehabilitation, The Fifth Affiliated Hospital of Zhengzhou University, No.3 Rehabilitation Street, Zhengzhou, 450052, People's Republic of China.
Ruijuan ZhengDepartment of Children Rehabilitation, The Fifth Affiliated Hospital of Zhengzhou University, No.3 Rehabilitation Street, Zhengzhou, 450052, People's Republic of China.
Pengya FengDepartment of Children Rehabilitation, The Fifth Affiliated Hospital of Zhengzhou University, No.3 Rehabilitation Street, Zhengzhou, 450052, People's Republic of China.
Cuixiang XuDepartment of Children Rehabilitation, The Fifth Affiliated Hospital of Zhengzhou University, No.3 Rehabilitation Street, Zhengzhou, 450052, People's Republic of China.
Enyao LiDepartment of Children Rehabilitation, The Fifth Affiliated Hospital of Zhengzhou University, No.3 Rehabilitation Street, Zhengzhou, 450052, People's Republic of China. enyao_li@yeah.net.
Liguo LiDepartment of Rehabilitation Medicine, Zhengzhou Health Vocational College, No. 69 Jingxiang Road, Zhengzhou, 450000, People's Republic of China. liguo_li@126.com.
Fifth Affiliated Hospital of Zhengzhou University · CNZhengzhou University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorder (ASD) is a neurodevelopmental disorder that cannot be cured. The ASD rat model was developed in this study to demonstrate the role and mechanism of ganglioside GM1 (GM1). Rats were given valproic acid (VPA) to create the ASD rat model. The rats' behaviors were assessed using the Y-maze test, open-field test, three-chamber social interaction test, and Morris water maze test. Relative levels of glutathione (GSH), malondialdehyde (MDA), catalase (CAT), reactive oxygen species (ROS), and superoxide dismutase (SOD) were quantitated using relative kits. Nissl, TUNEL, immunofluorescent, and immunohistochemistry staining techniques were used. GM1 treatment improved the ASD model rats' behavior disorders, including locomotor activity and exploratory behavior, social interaction, learning and memory capacity, and repetitive behavior. Following GM1 injection, striatal neurons grew and apoptosis decreased. GM1 reduced the excessively elevated α-Syn in ASD by encouraging autophagy. The behavior disorder of ASD model rats was exacerbated by autophagy inhibition, which also increased α-Syn levels. By increasing autophagy, GM1 reduced α-Syn levels and, ultimately, improved behavioral abnormalities in ASD model rats.

Indexed as

Autism Spectrum DisorderPrenatal Exposure Delayed EffectsAnimalsAutophagyDisease Models, AnimalFemaleG(M1) GangliosideHumansMaze LearningRatsSocial BehaviorValproic AcidG(M1) GangliosideValproic AcidASDAutophagyGM1α-Syn

Identifiers

PMID37084025
OpenAlexW4366602510

What Socratic holds

Textmetadata
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.