Evidence map›Paper›PMID 25869805›Full record

ArticleMolecular psychiatry2015

Targeting the schizophrenia genome: a fast track strategy from GWAS to clinic.

T Lencz, A K Malhotra

Abstract read
In one paragraph

Article in Molecular psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing 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

51 citing papers in PubMed.

  1. Article
  2. Autoantibodies and Inflammation in Schizophrenia.Psychiatry and clinical neurosciences · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Cortical morphological heterogeneity of schizophrenia and its relationship with glutamatergic receptor variations.European psychiatry : the journal of the Association of European Psychiatrists · 2023
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Identifying nootropic drug targets via large-scale cognitive GWAS and transcriptomics.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  15. Article
  16. Review
  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.

T Lencz1] Division of Psychiatry Research, Zucker Hillside Hospital, Glen Oaks, NY, USA [2] Center for Psychiatric Neuroscience, Feinstein Institute for Medical Research, Manhasset, NY, USA [3] Departments of Psychiatry and Molecular Medicine, Hofstra University School of Medicine, Hempstead, NY, USA.
A K Malhotra1] Division of Psychiatry Research, Zucker Hillside Hospital, Glen Oaks, NY, USA [2] Center for Psychiatric Neuroscience, Feinstein Institute for Medical Research, Manhasset, NY, USA [3] Departments of Psychiatry and Molecular Medicine, Hofstra University School of Medicine, Hempstead, NY, USA.

Funding

Next Generation Sequencing for Disease Mapping in a Founder PopulationR01MH095458 · NIMH · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI DARVASI, ARIEL, LENCZ, TODD · 2013 to 2016
$3.8M
NIMH NIH HHS R01 MH095458
6 · The paper itself

Abstract

The Psychiatric Genomics Consortium-Schizophrenia Workgroup (PGC-SCZ) has recently published a genomewide association study (GWAS) identifying >100 genetic loci, encompassing a total of 341 protein-coding genes, attaining genomewide significance for susceptibility to schizophrenia. Given the extremely long time (12-15 years) and expense (>$1 billion) associated with the development of novel drug targets, repurposing of drugs with known and validated targets may be the most expeditious path toward deriving clinical utility from these GWAS findings. In the present study, we examined all genes within loci implicated by the PGC-SCZ GWAS against databases of targets of both approved and registered pharmaceutical compounds. We identified 20 potential schizophrenia susceptibility genes that encode proteins that are the targets of approved drugs. Of these, we prioritized genes/targets that are of clear neuropsychiatric interest and that are also sole members of the linkage disequilibrium block surrounding a PGC-SCZ GWAS hit. In addition to DRD2, 5 genes meet these criteria: CACNA1C, CACNB2, CACNA1I, GRIN2A and HCN1. An additional 20 genes coding for proteins that are the targets of drugs in registered clinical trials, but without approved indications, were also identified. Although considerable work is still required to fully explicate the biological implications of the PGC-SCZ GWAS results, pathways related to these known, druggable targets may represent a promising starting point.

Indexed as

Genetic Predisposition to DiseaseAntipsychotic AgentsAsian PeopleClinical Trials as TopicDatabases, GeneticDatabases, PharmaceuticalGenome-Wide Association StudyHumansPharmacogeneticsSchizophreniaWhite PeopleAntipsychotic Agents

Identifiers

PMID25869805
PMCPMC4486648

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.