Evidence map›Paper›PMID 25805966›Full record

ReviewFrontiers in neuroscience2015

Neuronal migration abnormalities and its possible implications for schizophrenia.

Kazue Muraki, Kenji Tanigaki

Abstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
–field-weighted citation impact
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. Primary cilia and neural computation.Journal of biomedical science · 2026
    Review
  2. Loss of function of the chromatin remodeling geneProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. A body map of super-enhancers and their function in pig.Frontiers in veterinary science · 2023
    Article
  11. Article
  12. Downregulation of the schizophrenia risk-gene Dgcr2 alters early microcircuit development in the mouse medial prefrontal cortex.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2022
    Article
  13. Article
  14. Article
  15. ULK4 in Neurodevelopmental and Neuropsychiatric Disorders.Frontiers in cell and developmental biology · 2022
    Review
  16. Article
  17. Review
  18. Complement component C4 levels in the cerebrospinal fluid and plasma of patients with schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  19. Article
  20. Short-Term Effect of MgSOJournal of molecular neuroscience : MN · 2021
    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.

Kazue MurakiShiga Medical Center, Research Institute Moriyama, Shiga, Japan.
Kenji TanigakiShiga Medical Center, Research Institute Moriyama, Shiga, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia is a complex mental disorder that displays behavioral deficits such as decreased sensory gating, reduced social interaction and working memory deficits. The neurodevelopmental model is one of the widely accepted hypotheses of the etiology of schizophrenia. Subtle developmental abnormalities of the brain which stated long before the onset of clinical symptoms are thought to lead to the emergence of illness. Schizophrenia has strong genetic components but its underlying molecular pathogenesis is still poorly understood. Genetic linkage and association studies have identified several genes involved in neuronal migrations as candidate susceptibility genes for schizophrenia, although their effect size is small. Recent progress in copy number variation studies also has identified much higher risk loci such as 22q11. Based on these genetic findings, we are now able to utilize genetically-defined animal models. Here we summarize the results of neurodevelopmental and behavioral analysis of genetically-defined animal models. Furthermore, animal model experiments have demonstrated that embryonic and perinatal neurodevelopmental insults in neurogenesis and neuronal migrations cause neuronal functional and behavioral deficits in affected adult animals, which are similar to those of schizophrenic patients. However, these findings do not establish causative relationship. Genetically-defined animal models are a critical approach to explore the relationship between neuronal migration abnormalities and behavioral abnormalities relevant to schizophrenia.

Indexed as

22q11 deletion syndromeCxcr4Dgcr8DISC1GABAergic interneuronmouse modelsNeuregulin1schizophrenia

Identifiers

PMID25805966
PMCPMC4354421

What OpenQuestion holds

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Registered trials

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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.