Evidence map›Paper›PMID 21382468›Full record

ReviewInternational journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience2011

Synaptic changes in the brain of subjects with schizophrenia.

Gábor Faludi, Károly Mirnics

Abstract readReview
In one paragraph

Review in International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
4.4field-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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. The Potential of Hair Matrix for Biomarker Analysis in Schizophrenia.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Impaired copper transport in schizophrenia results in a copper-deficient brain state: A new side to the dysbindin story.The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry · 2020
    Article
  14. Article
  15. Article
  16. NMDAR Hypofunction Animal Models of Schizophrenia.Frontiers in molecular neuroscience · 2019
    Review
  17. Article
  18. How Memory Conforms to Brain Development.Frontiers in computational neuroscience · 2019
    Article
  19. Active Inference and Auditory Hallucinations.Computational psychiatry (Cambridge, Mass.) · 2018
    Article
  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

2 authors at 2 institutions in 2 countries.

Gábor FaludiDepartment of Psychiatry, Kútvölgyi Clinical Centre, Semmelweis University, Budapest, Hungary.
Károly Mirnics
Semmelweis University · HUVanderbilt University · US

Funding

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
NIMH NIH HHS R01 MH067234NIMH NIH HHS R01MH067234NIMH NIH HHS R01 MH079299NIMH NIH HHS R01MH079299
6 · The paper itself

Abstract

Clinical, epidemiological, neuroimaging and postmortem data all suggest schizophrenia is a neurodevelopmental disorder, and that synaptic disturbances might play a critical role in developing the disease. In 1982, Feinberg proposed that the schizophrenia might arise as a result of abnormal synaptic pruning. His hypothesis has survived 40years of accumulated data, and we review the critical findings related to synaptic dysfunction of schizophrenia. While it is clear that synaptic disturbances are integral and important for understanding the pathophysiology of schizophrenia, it has also become obvious that synaptic disturbances cannot be studied and understood as an independent disease hallmark, but only as a part of a complex network of homeostatic events. Development, glial-neural interaction, changes in energy homeostasis, diverse genetic predisposition, neuroimmune processes and environmental influences all can tip the delicate homeostatic balance of the synaptic morphology and connectivity in a uniquely individual fashion, thus contributing to the emergence of the various symptoms of this devastating disorder. Finally, we argue that based on a predominant change in gene expression pattern we can broadly sub-stratify schizophrenia into "synaptic" "oligodendroglial", "metabolic" and "inflammatory" subclasses.

Indexed as

AnimalsHumansSchizophreniaSynapses

Identifiers

PMID21382468
PMCPMC3074034
OpenAlexW2043611111

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.