Evidence map›Paper›PMID 18335162›Full record

ArticleJournal of neural transmission (Vienna, Austria : 1996)2008

Comprehensive analysis of polymorphisms throughout GAD1 gene: a family-based association study in schizophrenia.

J Du, S Duan, H Wang, W Chen, X Zhao, A Zhang, L Wang, J Xuan, L Yu, S Wu and 6 more

Abstract read
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In one paragraph

Article in Journal of neural transmission (Vienna, Austria : 1996), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 37 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Beyond the γ-aminobutyric acid hypothesis of schizophrenia.Frontiers in cellular neuroscience · 2023
    Review
  5. Article
  6. Review
  7. The Effects of Gene Variations ofPharmacogenomics and personalized medicine · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Expression of GABA signaling molecules KCC2, NKCC1, and GAD1 in cortical development and schizophrenia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  16. Genetic modulation of GABA levels in the anterior cingulate cortex by GAD1 and COMT.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2010
    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

16 authors at 3 institutions in 1 country.

J DuBio-X Center, Shanghai JiaoTong University, Shanghai, People's Republic of China.
S Duan
H Wang
W Chen
X Zhao
A Zhang
L Wang
J Xuan
L Yu
S Wu
W Tang
X Li
H Li
G Feng
Q Xing
L He
Chinese Academy of Sciences · CNShanghai Jiao Tong University · CNShanghai Mental Health Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies suggest that GAD1 gene is a functional candidate susceptibility gene for schizophrenia. In order to investigate the contribution of GAD1 gene to the etiology of schizophrenia in Chinese, we carried out a family-based association study between GAD1 gene and schizophrenia in 235 Chinese Han family trios. The GAD1 gene is comprehensively analyzed using a systematic mutation scan and the following-up association studies between common SNPs and schizophrenia in both single-locus and haplotype levels. Altogether, we have found 17 variants including 10 SNPs in 5'-flanking regions, 4 SNPs and one novel in-del in intronic regions and 2 SNPs (one novel SNP) in the 3'-untranslated region (UTR). Using the transmission disequilibrium test of the 9 common SNPs out of 17 variants, Significant evidence of SNP rs3791878-G allele in 5'-flanking region of GAD1 was preferentially transmitted to both the all offsprings of the trios (P = 0.0063, respectively; odds ratio = 1.83; 95% confidence interval: 1.26-2.65) and the male offsprings the trios (P = 0.0045, respectively; odds ratio = 2.21; 95% confidence interval: 1.37-3.56). Haplotype analysis suggested that rs3762556(C)-rs3791878(G)-rs6755102(C) is the major risky haplotype preferentially transmitted in both all the trios and male-offspring trios (Global P = 0.016 and 0.012, respectively). The gender-dependent of the risk of SNP rs3791878 suggest the complexity of GAD1 gene in schizophrenia. Given that the switch from G to T in SNP rs3791878 might cause the loss of ARNT and XBP1 transcriptional factor binding sites using a bioinformatics approach, our positive findings of this SNP support the hypothesis that the abruption of GAD1 gene is important to the risk of schizophrenia.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAdultFemaleGlutamate DecarboxylaseHumansMalePedigreePolymerase Chain ReactionSchizophreniaSex FactorsGlutamate Decarboxylaseglutamate decarboxylase 1

Identifiers

PMID18335162
OpenAlexW2045915489

What OpenQuestion holds

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Read underepoch 390

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.