Evidence map›Paper›PMID 21399908›Full record

ArticleNeurochemical research2011

Mice lacking major brain gangliosides develop parkinsonism.

Gusheng Wu, Zi-Hua Lu, Neil Kulkarni, Ruchi Amin, Robert W Ledeen

Open access · hybridAbstract read
In one paragraph

Article in Neurochemical research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
5.1field-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

68 citing papers in PubMed, 109 citations in OpenAlex.

  1. Review
  2. Review
  3. Amyloid β-Induced Inflammarafts in Alzheimer's Disease.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. GM1 oligosaccharide efficacy against α-synuclein aggregation and toxicity in vitro.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2023
    Article
  13. Article
  14. Ganglioside GM1 and the Central Nervous System.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Gangliosides in Neurodegenerative Diseases.Advances in neurobiology · 2023
    Article
  19. Review
  20. Review

8 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

5 authors at 2 institutions in 1 country.

Gusheng WuDepartment of Neurology and Neurosciences, New Jersey Medical School, UMDNJ, 185 So. Orange Ave., MSB-H506, Newark, NJ 07103, USA. ledeenro@umdnj.edu
Zi-Hua Lu
Neil Kulkarni
Ruchi Amin
Robert W Ledeen
Rutgers New Jersey Medical SchoolRutgers, The State University of New Jersey · US

Funding

Role of Nuclear Gangliosides in Neuronal FunctionR01NS033912 · NINDS · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI LEDEEN, ROBERT W · 1996 to 2012
$3.8M
NINDS NIH HHS 2R01 NS33912NINDS NIH HHS R01 NS033912
6 · The paper itself

Abstract

Parkinson's disease (PD) is the second most prevalent late-onset neurodegenerative disorder that affects nearly 1% of the global population aged 65 and older. Whereas palliative treatments are in use, the goal of blocking progression of motor and cognitive disability remains unfulfilled. A better understanding of the basic pathophysiological mechanisms underlying PD would help to advance that goal. The present study provides evidence that brain ganglioside abnormality, in particular GM1, may be involved. This is based on use of the genetically altered mice with disrupted gene Galgt1 for GM2/GD2 synthase which depletes GM2/GD2 and all the gangliotetraose gangliosides that constitute the major molecular species of brain. These knockout mice show overt motor disability on aging and clear indications of motor impairment with appropriate testing at an earlier age. This disability was rectified by L-dopa administration. These mice show other characteristic symptoms of PD, including depletion of striatal dopamine (DA), loss of DA neurons of the substantia nigra pars compacta, and aggregation of alpha synuclein. These manifestations of parkinsonism were largely attenuated by administration of LIGA-20, a membrane permeable analog of GM1 that penetrates the blood brain barrier and enters living neurons. These results suggest that perturbation of intracellular mechanisms mediated by intracellular GM1 may be a contributing factor to PD.

Indexed as

Brain ChemistryAgedalpha-SynucleinAnimalsBrainFemaleGangliosidesHumansMaleMiceMice, Inbred C57BLMice, KnockoutNeuronsNeuropsychological TestsParkinsonian DisordersPsychomotor Performancealpha-SynucleinGangliosides

Identifiers

PMID21399908
PMCPMC3155038
OpenAlexW2087713361

What OpenQuestion holds

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LicenceCC BY-NC
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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.