Literature DB >> 15642443

An association study between polymorphisms in five genes in glutamate and GABA pathway and paranoid schizophrenia.

Boyu Zhang1, Yanbo Yuan, Yanbin Jia, Xin Yu, Qi Xu, Yucun Shen, Yan Shen.   

Abstract

Dysfunctions of glutamatergic and GABAergic neurotransmission are two important hypotheses for the pathogenesis of schizophrenia. Thus, genes in the pathway are candidates for schizophrenia susceptibility. Phosphate-activated glutaminase (GLS), glutamine synthetase (GLUL), glutamic acid decarboxylase (GAD), GABA transaminase (ABAT) and succinic semialdehyde dehydrogenase (ALDH5A1) are five primary enzymes in glutamate and GABA synthetic and degradative pathway. In order to investigate the possible involvement of these genes in the development of paranoid schizophrenia, we genotyped 80 paranoid schizophrenics from northern China and 108 matched controls by polymerase chain reaction (PCR) and restriction fragment length polymorphisms (RFLP) methods or directly sequencing of PCR product. Seven SNPs were found to be polymorphic in the population investigated. No significant differences in the genotype distributions or allele frequencies between patients and controls were found. Therefore, we conclude the polymorphisms studied in the five genes do not play major roles in pathogenesis of paranoid schizophrenia in the population investigated.

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Year:  2005        PMID: 15642443     DOI: 10.1016/j.eurpsy.2004.09.028

Source DB:  PubMed          Journal:  Eur Psychiatry        ISSN: 0924-9338            Impact factor:   5.361


  6 in total

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

Authors:  J Du; 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
Journal:  J Neural Transm (Vienna)       Date:  2008-03-12       Impact factor: 3.575

2.  Relationship between genetic variation in the glutaminase gene GLS1 and brain glutamine/glutamate ratio measured in vivo.

Authors:  Dost Öngür; Stephen Haddad; Andrew P Prescot; J Eric Jensen; Richie Siburian; Bruce M Cohen; Perry F Renshaw; Jordan W Smoller
Journal:  Biol Psychiatry       Date:  2011-03-31       Impact factor: 13.382

3.  Glutaminase-deficient mice display hippocampal hypoactivity, insensitivity to pro-psychotic drugs and potentiated latent inhibition: relevance to schizophrenia.

Authors:  Inna Gaisler-Salomon; Gretchen M Miller; Nao Chuhma; Sooyeon Lee; Hong Zhang; Farhad Ghoddoussi; Nicole Lewandowski; Stephen Fairhurst; Yvonne Wang; Agnès Conjard-Duplany; Justine Masson; Peter Balsam; René Hen; Ottavio Arancio; Matthew P Galloway; Holly M Moore; Scott A Small; Stephen Rayport
Journal:  Neuropsychopharmacology       Date:  2009-06-10       Impact factor: 7.853

4.  How high-resolution basal-state functional imaging can guide the development of new pharmacotherapies for schizophrenia.

Authors:  Inna Gaisler-Salomon; Scott A Schobel; Scott A Small; Stephen Rayport
Journal:  Schizophr Bull       Date:  2009-10-14       Impact factor: 9.306

5.  GAD67 deficiency in parvalbumin interneurons produces deficits in inhibitory transmission and network disinhibition in mouse prefrontal cortex.

Authors:  Matthew S Lazarus; Keerthi Krishnan; Z Josh Huang
Journal:  Cereb Cortex       Date:  2013-11-24       Impact factor: 5.357

6.  Gene expression in cortical interneuron precursors is prescient of their mature function.

Authors:  Renata Batista-Brito; Robert Machold; Corinna Klein; Gord Fishell
Journal:  Cereb Cortex       Date:  2008-02-03       Impact factor: 5.357

  6 in total

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