Evidence map›Paper›PMID 31182727›Full record

ArticleScientific reports2019

GM1 Ganglioside Modifies α-Synuclein Toxicity and is Neuroprotective in a Rat α-Synuclein Model of Parkinson's Disease.

Jay S Schneider, Radha Aras, Courtney K Williams, James B Koprich, Jonathan M Brotchie, Vikrant Singh

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Sialylation in the nervous system: Functions and mechanisms.The Journal of biological chemistry · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Synucleinopathies: Intrinsic and Extrinsic Factors.Cell biochemistry and biophysics · 2023
    Article
  17. GM1 oligosaccharide efficacy against α-synuclein aggregation and toxicity in vitro.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2023
    Article
  18. Review
  19. Article
  20. 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

6 authors at 2 institutions in 2 countries.

Jay S SchneiderDepartment of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, 19107, USA. jay.schneider@jefferson.edu.
Radha ArasDepartment of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, 19107, USA.
Courtney K WilliamsDepartment of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, 19107, USA.
James B KoprichToronto Western Research Institute, Toronto Western Hospital, University Health Network, Toronto, Ontario, M5T 2S8, Canada.
Jonathan M BrotchieToronto Western Research Institute, Toronto Western Hospital, University Health Network, Toronto, Ontario, M5T 2S8, Canada.
Vikrant SinghDepartment of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, 19107, USA.
Thomas Jefferson University · USToronto Western Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While GM1 may interact with α-synuclein in vitro to inhibit aggregation, the ability of GM1 to protect against α-synuclein toxicity in vivo has not been investigated. We used targeted adeno-associated viral vector (AAV) overexpression of human mutant α-synuclein (A53T) in the rat substantia nigra (SN) to produce degeneration of SN dopamine neurons, loss of striatal dopamine levels, and behavioral impairment. Some animals received daily GM1 ganglioside administration for 6 weeks, beginning 24 hours after AAV-A53T administration or delayed start GM1 administration for 5 weeks beginning 3 weeks after AAV-A53T administration. Both types of GM1 administration protected against loss of SN dopamine neurons and striatal dopamine levels, reduced α-synuclein aggregation, and delayed start administration of GM1 reversed early appearing behavioral deficits. These results extend prior positive results in MPTP models, are consistent with the results of a small clinical study of GM1 in PD patients that showed slowing of symptom progression with chronic use, and argue for the continued refinement and development of GM1 as a potential disease modifying therapy for PD.

Indexed as

alpha-SynucleinAnimalsBehavior, AnimalCorpus StriatumDependovirusDisease Models, AnimalDopamineDopaminergic NeuronsGene Expression RegulationGenetic VectorsG(M1) GangliosideHumansNeuroprotective AgentsParkinson DiseaseRatsSubstantia Nigraalpha-SynucleinDopamineG(M1) GangliosideNeuroprotective AgentsSNCA protein, human

Identifiers

PMID31182727
PMCPMC6557812
OpenAlexW2950103628

What OpenQuestion 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 OpenQuestion graph.