Evidence map›Paper›PMID 28497346›Full record

ArticleNeurochemical research2017

Enhanced Autophagy Contributes to Protective Effects of GM1 Ganglioside Against Aβ1-42-Induced Neurotoxicity and Cognitive Deficits.

Ruwei Dai, Shijie Zhang, Wenjun Duan, Renrong Wei, Huifang Chen, Weibin Cai, Lei Yang, Qi Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

  1. Gangliosides in molecular interactions and cell regulation.The Journal of biological chemistry · 2026
    Review
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  9. Glycosphingolipids.Advances in experimental medicine and biology · 2021
    Article
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  11. Article
  12. Review
  13. Article
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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

8 authors at 1 institution in 1 country.

Ruwei DaiInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, No. 12 Jichang Road, Guangzhou, 510405, Guangdong, People's Republic of China.
Shijie ZhangInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, No. 12 Jichang Road, Guangzhou, 510405, Guangdong, People's Republic of China.
Wenjun DuanInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, No. 12 Jichang Road, Guangzhou, 510405, Guangdong, People's Republic of China.
Renrong WeiInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, No. 12 Jichang Road, Guangzhou, 510405, Guangdong, People's Republic of China.
Huifang ChenInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, No. 12 Jichang Road, Guangzhou, 510405, Guangdong, People's Republic of China.
Weibin CaiInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, No. 12 Jichang Road, Guangzhou, 510405, Guangdong, People's Republic of China.
Lei YangInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, No. 12 Jichang Road, Guangzhou, 510405, Guangdong, People's Republic of China. yanglei@gzucm.edu.cn.
Qi WangInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, No. 12 Jichang Road, Guangzhou, 510405, Guangdong, People's Republic of China. wanqi@gzucm.edu.cn.
Guangzhou University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder. The aggregation of Aβ peptides, Aβ1-42 in particular, is thought to be a fundamental pathogenic mechanism leading to the neuronal damage in AD. Recently, monosialoganglioside GM1 is reported to possess pivotal neuroprotection in neurodegenerative diseases. Previous studies have focused on the conformational dynamics and the biochemical interaction of the amyloid-peptide with the GM1 ganglioside, as well as the protective effect of GM1 on cognition. However, the phenomenon of autophagy with regard to neuronal dysfunction in AD is less investigated. In the present study, GM1 treatment were investigated in an AD mouse model and cultured PC12 dells to examine cognition-protective and neuroprotective effects of GM1. Furthermore, GM1 was found to induce autophagy via testing light chain 3 (LC3), Beclin1, neighbor of BRCA1 gene 1 protein and p62 (a substrate of LC3). Chloroquine, an inhibitor of lysosomal, was used to exclude the interference of lysosome, which could fuse with autophagosome and then clear it. In the presence of the inhibitor of autophagy (3-methyladenine; 3-MA), the protective effect of GM1 on PC12 cells in Aβ (1-42) induced toxic conditions was diminished. Interestingly, the expression of histone deacetylase 1 was increased in PC12 cells when treated with GM1, indicating that autophagy might be activated by GM1 through a pathway integrates protein acetylation. This study provides a novel insight into the protective role of GM1 against Aβ (1-42)-induced neurotoxicity via enhancing autophagy.

Indexed as

Amyloid beta-PeptidesAnimalsAutophagyCognitive DysfunctionDose-Response Relationship, DrugG(M1) GangliosideMaleMiceNeuronsNeuroprotective AgentsPC12 CellsPeptide FragmentsRandom AllocationRatsAmyloid beta-Peptidesamyloid beta-protein (1-42)G(M1) GangliosideNeuroprotective AgentsPeptide FragmentsAlzheimer’s diseaseAmyloid β-peptideAutophagyGM1 gangliosideNeuroprotection

Identifiers

PMID28497346
OpenAlexW2611983381

What OpenQuestion 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 OpenQuestion graph.