Evidence map›Paper›PMID 27754856›Full record

ArticleGenetics2016

Integrated Post-GWAS Analysis Sheds New Light on the Disease Mechanisms of Schizophrenia.

Jhih-Rong Lin, Ying Cai, Quanwei Zhang, Wen Zhang, Rubén Nogales-Cadenas, Zhengdong D Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.5field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 52 citations in OpenAlex.

  1. Autoantibodies and Inflammation in Schizophrenia.Psychiatry and clinical neurosciences · 2025
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Toll-Like Receptor (Neuropsychiatric disease and treatment · 2023
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review
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

6 authors at 1 institution in 1 country.

Jhih-Rong LinDepartment of Genetics, Albert Einstein College of Medicine, Bronx, New York 10461.
Ying CaiDepartment of Genetics, Albert Einstein College of Medicine, Bronx, New York 10461.
Quanwei ZhangDepartment of Genetics, Albert Einstein College of Medicine, Bronx, New York 10461.
Wen ZhangDepartment of Genetics, Albert Einstein College of Medicine, Bronx, New York 10461.
Rubén Nogales-CadenasDepartment of Genetics, Albert Einstein College of Medicine, Bronx, New York 10461.
Zhengdong D ZhangDepartment of Genetics, Albert Einstein College of Medicine, Bronx, New York 10461 zhengdong.zhang@einstein.yu.edu.
Albert Einstein College of Medicine · US

Funding

2/5 International Consortium on Brain and Behavior in 22q11.2 Deletion SyndromeU01MH101720 · NIMH · EMORY UNIVERSITY · PI WARREN, STEPHEN T. · 2013 to 2016
$6.2M
Interpreting human enhancer variants with a network-regularized composite modelR01HG008153 · NHGRI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI ZHANG, ZHENGDONG · 2016 to 2018
$3.1M
NHGRI NIH HHS R01 HG008153NIMH NIH HHS U01 MH101720
6 · The paper itself

Abstract

Schizophrenia is a severe mental disorder with a large genetic component. Recent genome-wide association studies (GWAS) have identified many schizophrenia-associated common variants. For most of the reported associations, however, the underlying biological mechanisms are not clear. The critical first step for their elucidation is to identify the most likely disease genes as the source of the association signals. Here, we describe a general computational framework of post-GWAS analysis for complex disease gene prioritization. We identify 132 putative schizophrenia risk genes in 76 risk regions spanning 120 schizophrenia-associated common variants, 78 of which have not been recognized as schizophrenia disease genes by previous GWAS. Even more significantly, 29 of them are outside the risk regions, likely under regulation of transcriptional regulatory elements contained therein. These putative schizophrenia risk genes are transcriptionally active in both brain and the immune system, and highly enriched among cellular pathways, consistent with leading pathophysiological hypotheses about the pathogenesis of schizophrenia. With their involvement in distinct biological processes, these putative schizophrenia risk genes, with different association strengths, show distinctive temporal expression patterns, and play specific biological roles during brain development.

Indexed as

Genetic LociGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansPolymorphism, Single NucleotideSchizophreniadisease risk gene prioritizationGWASschizophrenia

Identifiers

PMID27754856
PMCPMC5161287
OpenAlexW2532117501

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.