Publications by authors named "Boyu Zhang"

GABA(B) receptor1 (GABA(B)R1) gene is one of the susceptibility genes for temporal lobe epilepsy (TLE). Recently, it is reported that the GABA(B)R1 polymorphism (G1465A) conferred a highly increased susceptibility to TLE. We performed a case-control study to confirm the findings.

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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.

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We performed an association study between three SNPs in the genes of 14-3-3 family and paranoid schizophrenia. SNP rs983583 G/A in the YWHAZ gene showed significant association with paranoid schizophrenia. Our study indicated that the YWHAZ gene was a potential susceptibility gene for paranoid schizophrenia in the population studied.

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We genotyped six SNPs in the genes of p450 family among paranoid schizophrenics and normal controls. All subjects are unrelated Han Chinese. Three showed polymorphic, and no significant differences in allele or genotype frequencies were detected between patients and controls.

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Several lines of evidence suggest that dysfunctions of neurotransmitters are associated with schizophrenia. DOPA decarboxylase (DDC) is an enzyme involved directly in the synthesis of dopamine and serotonin, and indirectly in the synthesis of noradrenaline. Therefore, the DDC gene can be considered a candidate gene for schizophrenia.

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Purpose: Temporal lobe epilepsy with hippocampal sclerosis (TLE-HS+) is one of the most common medically intractable epilepsies. Although the pathogenesis of HS+ still remains highly controversial, genetics may play a role as a predisposing factor. Previous evidence in a Japanese population shows that the homozygotes for allele 2 at position -511 of the interleukin (IL)-1 beta gene promoter region (IL-1 beta-511*2/2) confers susceptibility to the development of HS.

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