Positive association of the human frizzled 3 (<i>FZD3</i>) gene haplotype with schizophrenia in Chinese Han population

Zhang, Yanbo; Yu, Xin; Yuan, Yanbo; Ling, Yansu; Ruan, Yan; Si, Tianmei; Lu, Tianlian; Wu, Shengxi; Gong, Xiaohong; Zhu, Zhongjun; Yang, Jianzhong; Wang, Fei; Zhang, Dai

doi:10.1002/ajmg.b.30076

Cited by 41 publications

(37 citation statements)

References 27 publications

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“…All of the participants were Chinese Han descendants. A part of this sample has been used in our previous study [17]. The age of clinical symptoms onset (13-53 years, mean 25.67 years) was retrospectively estimated as the time of emergence of any schizophrenic symptoms according to the International Classification of Diseases-10.…”

Section: Methodsmentioning

confidence: 99%

“…The construction of 25 ml PCR reaction mixture and the condition of PCR amplification were performed to be the same as that reported in our previous study [17], with annealing temperatures of 55-621C. Fifteen microliter PCR products were digested completely with 2U of restriction enzyme (HaeIII for rs947267, BsrI for rs778294) and electrophoresed subsequently on 2-4% agarose gels stained with ethidium bromide.…”

Section: Methodsmentioning

confidence: 99%

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Association of G72/G30 polymorphisms with early-onset and male schizophrenia

Yue¹,

Z²,

Kang³

et al. 2006

NeuroReport

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To explore the e¡ect of G72/G30 polymorphisms on the clinical manifestations of schizophrenia, especially on the age at onset and sex of patients, we examined three single nucleotide polymorphisms in 216 schizophrenic patients and 321 healthy controls. Signi¢cant associations of schizophrenia with the A allele of rs947267 (P ¼ 0.012) and haplotype A-A-G (rs2391191-rs947267-rs778294) (P ¼ 0.008) were found in early-onset schizophrenic patients. So did the same allele (P ¼ 0.034) and haplotype (P ¼ 0.009) as mentioned above in male patients. These ¢ndings suggest that the G72/G30 gene may modulate the age at onset and there might be a potential interaction between this locus and sex in the pathogenesis of schizophrenia. NeuroReport17:1899^1902 c 2006 Lippincott Williams & Wilkins.Keywords: age at onset, association study, G72/G30, polymorphism, schizophrenia IntroductionSchizophrenia is a major psychiatric disorder that affects almost 1% of the world's population and accounts for about 2.5% of healthcare costs [1]. Symptoms usually begin in late adolescence or early adulthood. Involvement of neurodevelopmental mechanism, especially glutamatergic transmission via N-methyl-D-aspartate receptors and synaptic plasticity in schizophrenia, has been recently suggested, on the basis of several lines of evidence [2]. Linkage analyses on diverse samples have provided accumulating evidence that chromosome 13q32-q33 may be involved in susceptibility to schizophrenia. A meta-analysis of genomewide linkage studies further identified 13q32-q33 as significantly linked to schizophrenia [3].Chumakov et al.[4] first reported that genetic variations near G72 (MIN 607408) and G30 (MIN 607415) locus on 13q34 were associated with schizophrenia in FrenchCanadian and Russian cohorts. G72 and G30 overlap on complementary chromosomal strands and are therefore transcribed in opposite directions. By yeast two-hybrid experiments, Chumakov et al.[4] also identified that the G72 protein interacts with the enzyme D-amino acid oxidase (MIN 124050), which regulates glutamatergic signaling through an N-methyl-D-aspartate receptor pathway. Gene expression analysis of G72 and G30 exhibited correlations between expression levels of the G72 and G30 genes, as well as a tendency toward overexpression of G72 mRNA in schizophrenic post-mortem dorsolateral prefrontal cortex of 44 schizophrenic patients compared with 44 control participants [5].Hattori et al. [6] suggested that a susceptibility variant for both bipolar illness and schizophrenia exists in the vicinity of the G72/G30 gene in two series of pedigrees. Findings from several subsequent studies tend to advance a role for G72/G30 in the overall risk for schizophrenia and bipolar disorder from various populations, including a metaanalysis study and a research based on a sample of childonset schizophrenia [7][8][9][10][11][12][13][14]. The majority of replication studies have, however, been inconsistent with respect to the associated alleles or haplotypes. Moreover, negative associations of G72/G30 pol...

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Association of G72/G30 polymorphisms with early-onset and male schizophrenia

Yue¹,

Z²,

Kang³

et al. 2006

NeuroReport

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“…The human FZD3 gene is located on chromosome 8p21, a linkage locus containing a putative gene for schizophrenia (Pulver et al, 1995;Blouin et al, 1998;Kendler et al, 2000;Gurling et al, 2001). Candidate gene association studies in this region have shown that SNPs within the FZD3 gene are strongly associated with schizophrenia in Chinese Han (Yang et al, 2003;Zhang et al, 2004), as well as in Japanese descents (Katsu et al, 2003). Nevertheless, such findings remain controversial since other groups have not been able to replicate and extend these observations in other populations (Ide et al, 2004;Jeong et al, 2006).…”

Section: Schizophrenia and Polymorphisms In Frizzled 3 And Gsk3bmentioning

confidence: 99%

The ups and downs of Wnt signaling in prevalent neurological disorders

2006

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In order to function properly, the brain must be wired correctly during critical periods in early development. Mistakes in this process are hypothesized to occur in disorders like autism and schizophrenia. Later in life, signaling pathways are essential in maintaining proper communication between neuronal and non-neuronal cells, and disrupting this balance may result in disorders like Alzheimer's disease. The Wnt/b-catenin pathway has a well-established role in cancer. Here, we review recent evidence showing the involvement of Wnt/b-catenin signaling in neurodevelopment as well as in neurodegenerative diseases. We suggest that the onset/development of such pathological conditions may involve the additive effect of genetic variation within Wnt signaling components and of molecules that modulate the activity of this signaling cascade.

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“…Furthermore, the studies of allele-specific single-nucleotide polymorphism (SNP) provide detailed information of disease susceptibility alleles, genotypes or haplotype transmission, regardless major or minor alleles on multiple risk loci on chromosome. 1-4 Numerous family-based linkage or population-based studies have identified a large set of schizophrenia-associated loci; however, many have not been replicated either in a different ethnic background, 5,6 or in the same ethnic background but in a diverse geographical location. 7,8 Although the number of risk loci is rather large, only a small portion overlaps with the large cumulative pool of genes that have shown changes of expression in the disease state.…”

Section: Introductionmentioning

confidence: 99%

An integrated genomic analysis of gene-function correlation on schizophrenia susceptibility genes

Chu

Liu

2010

J Hum Genet

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Schizophrenia is a highly complex inheritable disease characterized by numerous genetic susceptibility elements, each contributing a modest increase in risk for the disease. Although numerous linkage or association studies have identified a large set of schizophrenia-associated loci, many are controversial. In addition, only a small portion of these loci overlaps with the large cumulative pool of genes that have shown changes of expression in schizophrenia. Here, we applied a genomic gene-function approach to identify susceptibility loci that show direct effect on gene expression, leading to functional abnormalities in schizophrenia. We carried out an integrated analysis by cross-examination of the literature-based susceptibility loci with the schizophrenia-associated expression gene list obtained from our previous microarray study (Journal of Human Genetics (2009) 54: 665-75) using bioinformatic tools, followed by confirmation of gene expression changes using qPCR. We found nine genes (CHGB, SLC18A2, SLC25A27, ESD, C4A/C4B, TCP1, CHL1 and CTNNA2) demonstrate gene-function correlation involving: synapse and neurotransmission; energy metabolism and defense mechanisms; and molecular chaperone and cytoskeleton. Our findings further support the roles of these genes in genetic influence and functional consequences on the development of schizophrenia. It is interesting to note that four of the nine genes are located on chromosome 6, suggesting a special chromosomal vulnerability in schizophrenia.

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Positive association of the human frizzled 3 (FZD3) gene haplotype with schizophrenia in Chinese Han population

Cited by 41 publications

References 27 publications

Association of G72/G30 polymorphisms with early-onset and male schizophrenia

Association of G72/G30 polymorphisms with early-onset and male schizophrenia

The ups and downs of Wnt signaling in prevalent neurological disorders

An integrated genomic analysis of gene-function correlation on schizophrenia susceptibility genes

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