Evidence map›Paper›PMID 20018737›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Gangliosides play pivotal roles in the regulation of complement systems and in the maintenance of integrity in nerve tissues.

Yuhsuke Ohmi, Orie Tajima, Yuki Ohkawa, Atsushi Mori, Yasuo Sugiura, Keiko Furukawa, Koichi Furukawa

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.4field-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

48 citing papers in PubMed, 99 citations in OpenAlex.

  1. Review
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  9. Article
  10. Ganglioside GM3 Synthase Deficiency in Mouse Models and Human Patients.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Article
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  14. Review
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  16. Article
  17. Dietary Polar Lipids and Cognitive Development: A Narrative Review.Advances in nutrition (Bethesda, Md.) · 2019
    Review
  18. 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

7 authors at 2 institutions in 1 country.

Yuhsuke OhmiDepartment of Biochemistry II, Nagoya University Graduate School of Medicine, Nagoya 466-0065, Japan.
Orie Tajima
Yuki Ohkawa
Atsushi Mori
Yasuo Sugiura
Keiko Furukawa
Koichi Furukawa
Chubu University · JPNagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gangliosides are considered to be essential in the maintenance and repair of nervous tissues; however, the mechanisms for neurodegeneration caused by ganglioside defects are unknown. We examined gene expression profiles in double knockout (DKO) mice of GM2/GD2 synthase and GD3 synthase genes and showed that the majority of complement genes and their receptors were up-regulated in cerebellum in DKO mice. Inflammatory reactions were demonstrated in those tissues by measuring up-regulated inflammatory cytokines, indicating the presence of complement activation and inflammation as reported in Alzheimer's disease. Immunoblotting of fractionated membrane extracts by sucrose density gradient revealed that complement-regulatory molecules such as decay-accelerating factor and CD59 were dispersed from glycolipid-enriched microdomain/rafts in DKO cerebellum. Immunohistostaining of these molecules showed disordered membrane localization. These results suggested that dysfunction of complement-regulatory molecules may be due to abnormal glycolipid-enriched microdomain/rafts that triggered complement activation, subsequent inflammation, and neurodegeneration in DKO mice. Generation of the triple KO mice lacking complement activity in addition to the two glycosyltransferases suggested that complement activation is involved in the inflammatory reactions and neurodegeneration caused by the ganglioside deficiency.

Indexed as

AnimalsCD55 AntigensCerebellumComplement C3Complement System ProteinsCytokinesGangliosidesGene Expression ProfilingHumansInflammation MediatorsMembrane MicrodomainsMiceMice, KnockoutN-AcetylgalactosaminyltransferasesNerve DegenerationNerve Tissuealpha-N-acetylneuraminate alpha-2,8-sialyltransferaseCD55 AntigensComplement C3Complement System ProteinsCytokinesGangliosidesInflammation MediatorsN-Acetylgalactosaminyltransferases(N-acetylneuraminyl)-galactosylglucosylceramide N-acetylgalactosaminyltransferaseRNA, MessengerSialyltransferases

Identifiers

PMID20018737
PMCPMC2792163
OpenAlexW1997600119

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.