Hashimoto

et al. (2011)

[70]

(46.5% male (773/890), mean age ± SD: 46.9 ± 20.7 years).

Was found significant associations of three SNPs (rs11820062: p0.00011, rs2306365: p0.0031, and rs7119750: p0.0080) with schizophrenia and stronger evidence for association in a multi-marker sliding window haplotype analysis (the lowest p0.00006).

Zhong et al. (2011) [2]

576 individuals diagnosed with schizophrenia (290 males, mean age = 35.3 ± 11.6; 286 females, mean

age = 32.7 ± 13.4) and 566 healthy control subjects (308 males, mean age = 29.1 ± 13.6; 258 females, mean age = 29.4 ± 13.4). All patients were diagnosed by the Psychiatry Department of the Affiliated Hospital of Xi’an Jiaotong University School of Medicine according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria for schizophrenia.

It was genotyped six single-nucleotide polymorphisms (SNPs) in this region of FXYD6 in 1142 Han Chinese subjects (576 cases and 566 controls), and performed an association analysis. Significant associations with schizophrenia and the marker rs11544201 (P = 0.0028) and the haplotype rs10790212-rs11544201 (global P = 0.005) were found.

Naz et al. (2011) [15]

Schizophrenia patients and in controls. One hundred patients with schizophrenia and 70 healthy controls participated in the present study.

It was examined the association between the neuregulin 1 and tumor necrosis factor-α (−308) gene polymorphism with schizophrenia. This association was performed on the basis of molecular biology to screen the mutations of neuregulin 1 and tumor necrosis factor-α (−308) gene in schizophrenic patients by polymorphism analysis. Statistical analysis of the observed data shows that there was an association (P = 0.003) between patient’s group and controls in terms of genotypes of single-nucleotide polymorphism 1 rather than single-nucleotide polymorphism 2 of neuregulin 1.

ChuanYuan et al. (2011) [19]

81 Chinese Va schizophrenic patients and 210 Chinese Va healthy subjects

The authors found that genetic variants of the FZD3 gene may affect susceptibility to schizophrenia in Chinese Han and Va populations.

Pelov et al. (2011) [98]

868 Israeli Jewish participants, of whom 286 were patients with SZ and 582 were healthy controls. SZ patients were included with information regarding ethnicity (Ashkenazi vs. non-Ashkenazi origin).

The results imply a model in which PTPN5 may play a role in normal cognitive functioning and contribute to aspects of the neuropathology of SZ.

Dow et al. (2011) [6]

Whole blood samples were randomly selected from 92 schizophrenia patients from both the Munich and Aberdeen subjects.

Imputation analysis refined association between ADAMTSL3 and schizophrenia, and highlighted additional common variants with similar levels of association. We evaluated the functional consequences of all variants identified by sequencing, or showing direct or imputed association. The strongest evidence for function remained with the originally associated variant, rs950169, suggesting that this variant may be causal of the association. Rare variants were also identified with possible functional impact.

Cerasa et al. (2011) [102]

One hundred and seven healthy individuals (Caucasian, age-range: 18 - 73) recruited from universities, community recreational centers and

hospital personnel from 2005 to 2009.

Surface-based analysis of the cortical mantle showed that the dysbindin haplotype was associated with structural differences in the medial orbitofrontal cortex, where the risk carriers showed the highest cortical thickness values and the non-risk carriers the lowest. This study extends previous evidence found on schizophrenic patients to the healthy population, demonstrating the influence of dysbindin risk variants on the neuronal architecture of a specific brain region relevant to the neuropathology of schizophrenia.

Saito et al. (2011) [120]

Subset of subjects (94 schizophrenia patients and 94 control subjects).

The study fails to provide evidence for the contribution of PEA15, ENTPD4, and GAS2L1 genes to the etiology of schizophrenia in the Japanese population.

Sun et al. (2011) [7]

555 unrelated patients with paranoid schizophrenia and 567 unrelated healthy controls. A second sample analyzed 73 drug-free patients.

Haplotypic association was found for the VNTR-rs6323, VNTR rs1137070, and VNTRrs6323-rs1137070 haplotypes in female subjects. Nevertheless, no significant change of the expression of MAOA mRNA was detected in either female or male patients with paranoid schizophrenia.

Kähler et al. (2011) [13]

Norwegian subset (98 cases; 177 control subjects) with structural magnetic resonance imaging data.

The present results suggest that effects on biosynthesis of the neuronal epitope HNK-1, through common B3GAT2 variation, could increase the risk of SCZ, possibly by decreasing cortical area.