Evidence map›Paper›PMID 36255681›Full record

ArticleAdvances in neurobiology2023

Neuronal Ganglioside and Glycosphingolipid (GSL) Metabolism and Disease : Cascades of Secondary Metabolic Errors Can Generate Complex Pathologies (in LSDs).

Roger Sandhoff, Konrad Sandhoff

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Article in Advances in neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
10.1field-weighted citation impact, top 1% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

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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

2 authors at 2 institutions in 1 country.

Roger SandhoffLipid Pathobiochemistry Group, German Cancer Research Center, Heidelberg, Germany.
Konrad SandhoffLIMES, c/o Kekule-Institute for Organic Chemistry and Biochemistry, University of Bonn, Bonn, Germany. sandhoff@uni-bonn.de.
German Cancer Research Center · DEUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycosphingolipids (GSLs) are a diverse group of membrane components occurring mainly on the surfaces of mammalian cells. They and their metabolites have a role in intercellular communication, serving as versatile biochemical signals (Kaltner et al, Biochem J 476(18):2623-2655, 2019) and in many cellular pathways. Anionic GSLs, the sialic acid containing gangliosides (GGs), are essential constituents of neuronal cell surfaces, whereas anionic sulfatides are key components of myelin and myelin forming oligodendrocytes. The stepwise biosynthetic pathways of GSLs occur at and lead along the membranes of organellar surfaces of the secretory pathway. After formation of the hydrophobic ceramide membrane anchor of GSLs at the ER, membrane-spanning glycosyltransferases (GTs) of the Golgi and Trans-Golgi network generate cell type-specific GSL patterns for cellular surfaces. GSLs of the cellular plasma membrane can reach intra-lysosomal, i.e. luminal, vesicles (ILVs) by endocytic pathways for degradation. Soluble glycoproteins, the glycosidases, lipid binding and transfer proteins and acid ceramidase are needed for the lysosomal catabolism of GSLs at ILV-membrane surfaces. Inherited mutations triggering a functional loss of glycosylated lysosomal hydrolases and lipid binding proteins involved in GSL degradation cause a primary lysosomal accumulation of their non-degradable GSL substrates in lysosomal storage diseases (LSDs). Lipid binding proteins, the SAPs, and the various lipids of the ILV-membranes regulate GSL catabolism, but also primary storage compounds such as sphingomyelin (SM), cholesterol (Chol.), or chondroitin sulfate can effectively inhibit catabolic lysosomal pathways of GSLs. This causes cascades of metabolic errors, accumulating secondary lysosomal GSL- and GG- storage that can trigger a complex pathology (Breiden and Sandhoff, Int J Mol Sci 21(7):2566, 2020).

Indexed as

GlycosphingolipidsLysosomal Storage DiseasesAcid CeramidaseAnimalsCeramidesCholesterolChondroitin SulfatesGangliosidesGlycoproteinsGlycoside HydrolasesGlycosyltransferasesMammalsN-Acetylneuraminic AcidSphingomyelinsSulfoglycosphingolipidsAcid CeramidaseCeramidesCholesterolChondroitin SulfatesGangliosidesGlycoproteinsGlycoside HydrolasesGlycosphingolipidsGlycosyltransferasesN-Acetylneuraminic AcidSphingomyelinsSulfoglycosphingolipidsAlzheimerCatabolismDegradationDevelopmentEndosomal pathwayFrontal lobe dementiaGanglio-seriesGangliosideGenetic diseaseGlycolipidGlycosphingolipidGlycosyltransferaseHydrolaseIntra-lysosomal luminal vesicle (ILV)Lysosomal storage disease (LSD)LysosomeMembrane-surfaceMetabolismNeurodegenerative diseaseNeuronOrganelleParkinsonReceptorSecondary storageSecretory pathwaySphingolipid-binding protein (SAP)Sphingolipid-transfer proteinTopology

Identifiers

PMID36255681
OpenAlexW4306729559

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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 OpenQuestion graph.