Evidence map›Paper›PMID 17089069›Full record

ArticleJournal of human genetics2007

Association and synergistic interaction between promoter variants of the DRD4 gene in Japanese schizophrenics.

Mizuho Nakajima, Eiji Hattori, Kazuo Yamada, Yoshimi Iwayama, Tomoko Toyota, Yasuhide Iwata, Kenji J Tsuchiya, Genichi Sugihara, Kenji Hashimoto, Hiroyuki Watanabe and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of human genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 24 citations in OpenAlex.

  1. Therapeutic potential ofIn silico pharmacology · 2026
    Article
  2. Article
  3. Genes · 2024
    Article
  4. A meta-analysis of data associatingNeuropsychiatric disease and treatment · 2018
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. 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

13 authors at 6 institutions in 1 country.

Mizuho NakajimaLaboratory for Molecular Psychiatry, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako-city, Saitama, 351-0198, Japan.
Eiji HattoriLaboratory for Molecular Psychiatry, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako-city, Saitama, 351-0198, Japan.
Kazuo YamadaLaboratory for Molecular Psychiatry, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako-city, Saitama, 351-0198, Japan.
Yoshimi IwayamaLaboratory for Molecular Psychiatry, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako-city, Saitama, 351-0198, Japan.
Tomoko ToyotaLaboratory for Molecular Psychiatry, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako-city, Saitama, 351-0198, Japan.
Yasuhide IwataDepartment of Psychiatry and Neurology, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, 431-3192, Japan.
Kenji J TsuchiyaDepartment of Psychiatry and Neurology, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, 431-3192, Japan.
Genichi SugiharaDepartment of Psychiatry and Neurology, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, 431-3192, Japan.
Kenji HashimotoDivision of Clinical Neuroscience, Chiba University, Center for Forensic Mental Health, Chiba, 260-8670, Japan.
Hiroyuki WatanabeDepartment of Psychiatry, Chiba University, Graduate School of Medicine, Chiba, Japan.
Masaomi IyoDepartment of Psychiatry, Chiba University, Graduate School of Medicine, Chiba, Japan.
Akinori HoshikaDepartment of Paediatrics, Tokyo Medical University, Shinjuku, Tokyo, 160-0023, Japan.
Takeo YoshikawaLaboratory for Molecular Psychiatry, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako-city, Saitama, 351-0198, Japan. takeo@brain.riken.jp.
RIKEN Center for Brain Science · JPHamamatsu University School of Medicine · JPChiba University · JPCenter for Forensic Mental Health, Chiba University · JPJapan Science and Technology Agency · JPTokyo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent association studies suggest that polymorphisms in the promoter and exon 1 upstream region of the dopamine D4 receptor (DRD4) gene play a functional role in the development of common psychiatric illnesses, although there are also conflicting results. In this study, we re-sequenced this region to identify all genomic variants, and tested them for association with schizophrenia. A total of 570 Japanese schizophrenic cases with matched controls were studied by genotyping all identified/validated common polymorphisms (-1106T>C, -906T>C, -809G>A, -616G>C, -521T>C, -376C>T, -291C>T and 12-bp repeat) and a known microsatellite (120-bp tandem duplication) in the upstream region. A single nucleotide polymorphism (SNP) -809G>A in the promoter region was found to be significantly associated with disease (P=0.018 and 0.032 for allelic and genotypic comparisons, respectively), although not surviving after Bonferroni correction. Logistic regression analysis showed that a combination of the four polymorphisms, -809G>A, -616G>C, -291C>T and the 12-bp repeat, conferred a susceptibility to schizophrenia. These results suggest that the upstream variants have a primary functional effect in the etiology of schizophrenia in the Japanese population.

Indexed as

Polymorphism, Single NucleotidePromoter Regions, GeneticExonsFemaleGenetic VariationGenotypeHaplotypesHumansJapanLogistic ModelsMaleMiddle AgedMolecular Sequence DataReceptors, Dopamine D4SchizophreniaDRD4 protein, humanReceptors, Dopamine D4

Identifiers

PMID17089069
PMCPMC1705471
OpenAlexW2137602939

What OpenQuestion holds

Textmetadata
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.