Evidence map›Paper›PMID 34757540›Full record

ReviewGlycoconjugate journal2022

Glycosphingolipid metabolism and its role in ageing and Parkinson's disease.

Kerri-Lee Wallom, María E Fernández-Suárez, David A Priestman, Danielle Te Vruchte, Mylene Huebecker, Penelope J Hallett, Ole Isacson, Frances M Platt

Open access · hybridAbstract readReview
In one paragraph

Review in Glycoconjugate journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Lack of significant ganglioside changes inBiochemistry and biophysics reports · 2025
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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.

Kerri-Lee WallomDepartment of Pharmacology, University of Oxford, Oxford, UK.ORCID 0000-0002-2842-1275
María E Fernández-SuárezDepartment of Pharmacology, University of Oxford, Oxford, UK.ORCID 0000-0003-4277-2079
David A PriestmanDepartment of Pharmacology, University of Oxford, Oxford, UK.ORCID 0000-0002-0030-0148
Danielle Te VruchteDepartment of Pharmacology, University of Oxford, Oxford, UK.ORCID 0000-0002-1709-1709
Mylene HuebeckerInstitute of Innate Immunity, Biophysical Imaging, Medical Faculty, University of Bonn, Bonn, Germany.ORCID 0000-0003-3030-7110
Penelope J HallettNeuroregeneration Institute, McLean Hospital, Harvard Medical School, Belmont, MA, 02478, USA.ORCID 0000-0002-8858-9096
Ole IsacsonNeuroregeneration Institute, McLean Hospital, Harvard Medical School, Belmont, MA, 02478, USA.ORCID 0000-0001-8091-8302
Frances M PlattDepartment of Pharmacology, University of Oxford, Oxford, UK. frances.platt@pharm.ox.ac.uk.ORCID 0000-0001-7614-0403
University of Oxford · GBHarvard University · USUniversity of Bonn · DE

Funding

Prevention of complement and immune-mediated Lewy body dementiaR01AG060195 · NIA · MCLEAN HOSPITAL · PI HALLETT, PENELOPE JANE, HASTINGS, MICHELLE L · 2018 to 2022
$2.9M
NIA NIH HHS R01 AG060195Wellcome Trust
6 · The paper itself

Abstract

It is well established that lysosomal glucocerebrosidase gene (GBA) variants are a risk factor for Parkinson's disease (PD), with increasing evidence suggesting a loss of function mechanism. One question raised by this genetic association is whether variants of genes involved in other aspects of sphingolipid metabolism are also associated with PD. Recent studies in sporadic PD have identified variants in multiple genes linked to diseases of glycosphingolipid (GSL) metabolism to be associated with PD. GSL biosynthesis is a complex pathway involving the coordinated action of multiple enzymes in the Golgi apparatus. GSL catabolism takes place in the lysosome and is dependent on the action of multiple acid hydrolases specific for certain substrates and glycan linkages. The finding that variants in multiple GSL catabolic genes are over-represented in PD in a heterozygous state highlights the importance of GSLs in the healthy brain and how lipid imbalances and lysosomal dysfunction are associated with normal ageing and neurodegenerative diseases. In this article we will explore the link between lysosomal storage disorders and PD, the GSL changes seen in both normal ageing, lysosomal storage disorders (LSDs) and PD and the mechanisms by which these changes can affect neurodegeneration.

Indexed as

Lysosomal Storage DiseasesParkinson DiseaseAgingGlucosylceramidaseGlycosphingolipidsHumansLysosomesMutationGlucosylceramidaseGlycosphingolipidsAgeingGangliosidesGBAGlycosphingolipid (GSL)Lysosomal storage disease (LSD)Parkinson’s disease (PD)

Identifiers

PMID34757540
PMCPMC8979855
OpenAlexW3205856331

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.