Evidence map›Paper›PMID 35933559›Full record

ArticleNPJ Parkinson's disease2022

Elevation of gangliosides in four brain regions from Parkinson's disease patients with a GBA mutation.

Shani Blumenreich, Tamar Nehushtan, Or B Barav, Jennifer T Saville, Tamir Dingjan, John Hardy, Maria Fuller, Anthony H Futerman

Open access · goldAbstract read
In one paragraph

Article in NPJ Parkinson's disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Rare-Variant Burden across Lysosomal Genes Implicates Sialylation and Ganglioside Metabolism in Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2026
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  8. Review
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  11. Review
  12. Article
  13. Article
  14. Lack of significant ganglioside changes inBiochemistry and biophysics reports · 2025
    Article
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  16. Article
  17. Article
  18. Review
  19. Review
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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 3 institutions in 3 countries.

Shani BlumenreichDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, 7610001, Israel.
Tamar NehushtanDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, 7610001, Israel.
Or B BaravDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, 7610001, Israel.
Jennifer T SavilleGenetics and Molecular Pathology, SA Pathology at Women's and Children's Hospital and Adelaide Medical School, The University of Adelaide, Adelaide, SA, 5005, Australia.
Tamir DingjanDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, 7610001, Israel.ORCID http://orcid.org/0000-0001-5782-3161
John HardyDepartment of Neurodegenerative Disease, UCL Dementia Research Institute, University College London, London, WC1N 3BG, UK.
Maria FullerGenetics and Molecular Pathology, SA Pathology at Women's and Children's Hospital and Adelaide Medical School, The University of Adelaide, Adelaide, SA, 5005, Australia.
Anthony H FutermanDepartment of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, 7610001, Israel. tony.futerman@weizmann.ac.il.ORCID http://orcid.org/0000-0003-0013-0115
Weizmann Institute of Science · ILSouth Australia Pathology · AUUK Dementia Research Institute · GB

Funding

Medical Research Council G0701075Medical Research Council G0901254Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation) 16132
6 · The paper itself

Abstract

A number of genetic risk factors have been identified over the past decade for Parkinson's Disease (PD), with variants in GBA prominent among them. GBA encodes the lysosomal enzyme that degrades the glycosphingolipid, glucosylceramide (GlcCer), with the activity of this enzyme defective in Gaucher disease. Based on the ill-defined relationship between glycosphingolipid metabolism and PD, we now analyze levels of various lipids by liquid chromatography/electrospray ionization-tandem mass spectrometry in four brain regions from age- and sex-matched patient samples, including idiopathic PD, PD patients with a GBA mutation and compare both to control brains (n = 21 for each group) obtained from individuals who died from a cause unrelated to PD. Of all the glycerolipids, sterols, and (glyco)sphingolipids (251 lipids in total), the only lipid class which showed significant differences were the gangliosides (sialic acid-containing complex glycosphingolipids), which were elevated in 3 of the 4 PD-GBA brain regions. There was no clear correlation between levels of individual gangliosides and the genetic variant in Gaucher disease [9 samples of severe (neuronopathic), 4 samples of mild (non-neuronopathic) GBA variants, and 8 samples with low pathogenicity variants which have a higher risk for development of PD]. Most brain regions, i.e. occipital cortex, cingulate gyrus, and striatum, did not show a statistically significant elevation of GlcCer in PD-GBA. Only one region, the middle temporal gyrus, showed a small, but significant elevation in GlcCer concentration in PD-GBA. We conclude that changes in ganglioside, but not in GlcCer levels, may contribute to the association between PD and GBA mutations.

Identifiers

PMID35933559
PMCPMC9357011
OpenAlexW4290026893

What Socratic holds

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Registered trials

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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.