Evidence map›Paper›PMID 19147160›Full record

ReviewJournal of the neurological sciences2009

Ceramide and neurodegeneration: susceptibility of neurons and oligodendrocytes to cell damage and death.

Arundhati Jana, Edward L Hogan, Kalipada Pahan

Open access · greenAbstract readReview
In one paragraph

Review in Journal of the neurological sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers.

0numbers the graph read from it
0cells of the map it votes in
129citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

129 citing papers in PubMed, 228 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Benzoate Drugs for Traumatic Brain Injury.Journal of clinical & experimental immunology · 2026
    Article
  8. Review
  9. Article
  10. IGFBP2-Ceramide Pathway Mediates Divergent Myelin Breakdown in the PNS and CNS Following Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  11. Review
  12. Article
  13. Structure of the yeast ceramide synthase.Nature structural & molecular biology · 2025
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

69 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

3 authors at 2 institutions in 1 country.

Arundhati JanaDepartment of Neurological sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Edward L Hogan
Kalipada Pahan
Rush University Medical Center · USAugusta University · US

Funding

ACTIVATION OF NF-KB IN GLIAL CELLS AND CNS OF EAER01NS039940 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI PAHAN, KALIPADA · 2001 to 2009
$2.7M
Infection in Multiple Sclerosis (MS)R21NS051666 · NINDS · AUGUSTA UNIVERSITY · PI HOGAN, EDWARD L. · 2006 to 2007
$361k
Statin and Phenylacetate in MPTP Mouse ModelR21NS048923 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI PAHAN, KALIPADA · 2006 to 2007
$327k
NINDS NIH HHS NS39940NINDS NIH HHS NS48923NINDS NIH HHS NS 51666NINDS NIH HHS R01 NS039940NINDS NIH HHS R21 NS048923NINDS NIH HHS R21 NS051666
6 · The paper itself

Abstract

Neurodegenerative disorders are marked by extensive neuronal apoptosis and gliosis. Although several apoptosis-inducing agents have been described, understanding of the regulatory mechanisms underlying modes of cell death is incomplete. A major breakthrough in delineation of the mechanism of cell death came from elucidation of the sphingomyelin (SM)-ceramide pathway that has received worldwide attention in recent years. The SM pathway induces apoptosis, differentiation, proliferation, and growth arrest depending upon cell and receptor types, and on downstream targets. Sphingomyelin, a plasma membrane constituent, is abundant in mammalian nervous system, and ceramide, its primary catabolic product released by activation of either neutral or acidic sphingomyelinase, serves as a potential lipid second messenger or mediator molecule modulating diverse cellular signaling pathways. Neutral sphingomyelinase (NSMase) is a key enzyme in the regulated activation of the SM cycle and is particularly sensitive to oxidative stress. In a context of increasing clarification of the mechanisms of neurodegeneration, we thought that it would be useful to review details of recent findings that we and others have made concerning different pro-apoptotic neurotoxins including proinflammatory cytokines, hypoxia-induced SM hydrolysis and ceramide production that induce cell death in human primary neurons and primary oligodendrocytes: redox sensitive events. What has and is emerging is a vista of therapeutically important ceramide regulation affecting a variety of different neurodegenerative and neuroinflammatory disorders.

Indexed as

ApoptosisAgingCell DifferentiationCeramidesCytokinesHumansMembrane MicrodomainsMitochondriaNerve DegenerationNervous System DiseasesNeurodegenerative DiseasesNeuronsNeurotoxinsOligodendrogliaOxidative StressSignal TransductionCeramidesCytokinesNeurotoxinsSphingomyelins

Identifiers

PMID19147160
PMCPMC2660887
OpenAlexW1969430540

What OpenQuestion holds

Textmetadata
LicenceTDM
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.