Evidence map›Paper›PMID 20127207›Full record

ReviewMolecular neurobiology2010

Deregulated sphingolipid metabolism and membrane organization in neurodegenerative disorders.

Marco Piccinini, Federica Scandroglio, Simona Prioni, Barbara Buccinnà, Nicoletta Loberto, Massimo Aureli, Vanna Chigorno, Elisa Lupino, Giovanni DeMarco, Annarosa Lomartire and 3 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

67 citing papers in PubMed, 137 citations in OpenAlex.

  1. Article
  2. Sphingolipids in Emotional Well-Being.Journal of neurochemistry · 2026
    Review
  3. Frontiers in nutrition · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
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  12. GBA-associated PD: chances and obstacles for targeted treatment strategies.Journal of neural transmission (Vienna, Austria : 1996) · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review

7 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

13 authors at 2 institutions in 1 country.

Marco PiccininiSection of Biochemistry, Department of Medicine and Experimental Oncology, University of Turin, Turin, Italy.
Federica Scandroglio
Simona Prioni
Barbara Buccinnà
Nicoletta Loberto
Massimo Aureli
Vanna Chigorno
Elisa Lupino
Giovanni DeMarco
Annarosa Lomartire
Maria Teresa Rinaudo
Sandro Sonnino
Alessandro Prinetti
University of Milan · ITUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sphingolipids are polar membrane lipids present as minor components in eukaryotic cell membranes. Sphingolipids are highly enriched in nervous cells, where they exert important biological functions. They deeply affect the structural and geometrical properties and the lateral order of cellular membranes, modulate the function of several membrane-associated proteins, and give rise to important intra- and extracellular lipid mediators. Sphingolipid metabolism is regulated along the differentiation and development of the nervous system, and the expression of a peculiar spatially and temporarily regulated sphingolipid pattern is essential for the maintenance of the functional integrity of the nervous system: sphingolipids in the nervous system participate to several signaling pathways controlling neuronal survival, migration, and differentiation, responsiveness to trophic factors, synaptic stability and synaptic transmission, and neuron-glia interactions, including the formation and stability of central and peripheral myelin. In several neurodegenerative diseases, sphingolipid metabolism is deeply deregulated, leading to the expression of abnormal sphingolipid patterns and altered membrane organization that participate to several events related to the pathogenesis of these diseases. The most impressive consequence of this deregulation is represented by anomalous sphingolipid-protein interactions that are at least, in part, responsible for the misfolding events that cause the fibrillogenic and amyloidogenic processing of disease-specific protein isoforms, such as amyloid beta peptide in Alzheimer's disease, huntingtin in Huntington's disease, alpha-synuclein in Parkinson's disease, and prions in transmissible encephalopathies. Targeting sphingolipid metabolism represents today an underexploited but realistic opportunity to design novel therapeutic strategies for the intervention in these diseases.

Indexed as

AnimalsCarbohydrate ConformationCarbohydrate SequenceCell MembraneHumansMolecular Sequence DataMolecular StructureMyelin SheathNeurodegenerative DiseasesPrion DiseasesSphingolipidosesSphingolipidsSphingolipids

Identifiers

PMID20127207
OpenAlexW2013374003

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.