Evidence map›Paper›PMID 24478629›Full record

ReviewFrontiers in cellular neuroscience2014

Schizophrenia: susceptibility genes and oligodendroglial and myelin related abnormalities.

Panos Roussos, Vahram Haroutunian

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
6.4field-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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. IncreasingBiological psychiatry global open science · 2025
    Article
  5. Repurposing medications to prevent psychosis.Npj mental health research · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. The Node of Ranvier as an Interface for Axo-Glial Interactions: Perturbation of Axo-Glial Interactions in Various Neurological Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023
    Review
  11. Investigation ofNagoya journal of medical science · 2022
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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 1 institution in 1 country.

Panos RoussosMental Illness Research, Education, and Clinical Center (VISN 3), James J. Peters VA Medical Center Bronx, NY, USA ; Department of Psychiatry, Icahn School of Medicine at Mount Sinai New York, NY, USA ; Department of Genetics and Genomic Science and Institute for Multiscale Biology, Icahn School of Medicine at Mount Sinai New York, NY, USA.
Vahram HaroutunianMental Illness Research, Education, and Clinical Center (VISN 3), James J. Peters VA Medical Center Bronx, NY, USA ; Department of Psychiatry, Icahn School of Medicine at Mount Sinai New York, NY, USA ; Department of Neuroscience, Icahn School of Medicine at Mount Sinai New York, NY, USA.
James J. Peters VA Medical Center · US

Funding

QUANTITATIVE ANALYSIS OF MICROVASCULAR CHANGES IN THE AGING BRAINP01AG002219 · NIA · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI HAROUTUNIAN, VAHRAM · 1985 to 2009
$19.2M
White Matter Abnormalities in SchizophreniaP50MH066392 · NIMH · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BUXBAUM, JOSEPH D. · 2002 to 2012
$18.6M
Cortico-thalamic Glutamate/GABA mRNA in schizophreniaR01MH064673 · NIMH · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI HAROUTUNIAN, VAHRAM · 2003 to 2012
$3.4M
Dissecting Cis Regulation of Gene Expression in SchizophreniaI01BX002395 · VA · JAMES J PETERS VA MEDICAL CENTER · PI ROUSSOS, PANAGIOTIS · 2014 to 2022
–
BLRD VA I01 BX002395NIMH NIH HHS P50 MH066392NIMH NIH HHS R01 MH064673
6 · The paper itself

Abstract

Given that the genetic risk for schizophrenia is highly polygenic and the effect sizes, even for rare or de novo events, are modest at best, it has been suggested that multiple biological pathways are likely to be involved in the etiopathogenesis of the disease. Most efforts in understanding the cellular basis of schizophrenia have followed a "neuron-centric" approach, focusing on alterations in neurotransmitter systems and synapse cytoarchitecture. However, multiple lines of evidence coming from genetics and systems biology approaches suggest that apart from neurons, oligodendrocytes and potentially other glia are affected from schizophrenia risk loci. Neurobiological abnormalities linked with genetic association signal could identify abnormalities that are more likely to be primary, versus environmentally induced changes or downstream events. Here, we summarize genetic data that support the involvement of oligodendrocytes in schizophrenia, providing additional evidence for a causal role with the disease. Given the undeniable evidence of both neuronal and glial abnormalities in schizophrenia, we propose a neuro-glial model that invokes abnormalities at the node of Ranvier as a functional unit in the etiopathogenesis of the disease.

Indexed as

disconnectivityGWASnode of Ranvierpolygenicsystems biology

Identifiers

PMID24478629
PMCPMC3896818
OpenAlexW1974665574

What OpenQuestion holds

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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.