Evidence map›Paper›PMID 24507510›Full record

ReviewBiological psychiatry2015

Schizophrenia as a disorder of molecular pathways.

Szatmár Horváth, Károly Mirnics

Open access · greenAbstract readReview
In one paragraph

Review in Biological psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. The Antipsychotic Drug Clozapine Suppresses the RGS4 Polyubiquitylation and Proteasomal Degradation Mediated by the Arg/N-Degron Pathway.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  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 2 institutions in 2 countries.

Szatmár HorváthDepartment of Psychiatry; Department of Psychiatry, University of Szeged, Szeged, Hungary.
Károly MirnicsDepartment of Psychiatry; Vanderbilt Kennedy Center for Research on Human Development, Vanderbilt University, Nashville, Tennessee; Department of Psychiatry, University of Szeged, Szeged, Hungary. Electronic address: karoly.mirnics@vanderbilt.edu.
John F. Kennedy Center for the Performing Arts · USUniversity of Szeged · HU

Funding

THREE-TIERED PREVENTION MODEL TO BETTER SERVE ALL STUDENP30HD015052 · NICHD · VANDERBILT UNIVERSITY · PI DYKENS, ELISABETH MAY · 1985 to 2014
$18.6M
Neocortical Transcriptome Changes in SchizophreniaR01MH067234 · NIMH · VANDERBILT UNIVERSITY · PI MIRNICS, KAROLY · 2003 to 2021
$4.7M
Neuroimmune Changes in SchizophreniaR01MH079299 · NIMH · VANDERBILT UNIVERSITY · PI MIRNICS, KAROLY · 2007 to 2011
$1.7M
NICHD NIH HHS P30 HD015052NIMH NIH HHS R01 MH067234NIMH NIH HHS R01MH067234NIMH NIH HHS R01 MH079299
6 · The paper itself

Abstract

Over the last decade, transcriptome studies of postmortem tissue from subjects with schizophrenia revealed that synaptic, mitochondrial, immune system, gamma-aminobutyric acidergic, and oligodendrocytic changes are all integral parts of the disease process. The combined genetic and transcriptomic studies argue that the molecular underpinnings of the disease are even more varied than the symptomatic diversity of schizophrenia. Ultimately, to decipher the pathophysiology of human disorders in general, we will need to understand the function of hundreds of genes and regulatory elements in our genome and the consequences of their overexpression and reduced expression in a developmental context. Furthermore, integration of knowledge from various data sources remains a monumental challenge that has to be systematically addressed in the upcoming decades. In the end, our success in interpreting the molecular changes in schizophrenia will depend on our ability to understand the biology using innovative ideas and cannot depend on the hope of developing novel, more powerful technologies.

Indexed as

Signal TransductionAnimalsGene-Environment InteractionGene ExpressionGenetic Predisposition to DiseaseHumansSchizophreniaTranscriptomeConvergenceGene ExpressionGene NetworkGeneticsPostmortemSchizophrenia

Identifiers

PMID24507510
PMCPMC4092052
OpenAlexW2061550475

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.