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In conclusion, this study demonstrates the functional impact of c.391 A > G variant and its biological effect makes it a good candidate as risk variant for schizophrenia.
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findings of this study provide some evidence that the NPSR1 and GAD1 polymorphisms might play a role in the development of war-related PTSD and its related psychological expressions; further research is needed to elucidate the interactions of specific gene variants and environmental factors in the development of PTSD
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Association between GAD1 rs3749034 polymorphisms with antisaccade task performance in schizophrenic patients.
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This study detected significant reductions in the mRNAs associated with GAD1 in the frontal cortex (FC) of autism spectrum disorder.
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Our results demonstrate a weak effect of the GAD1 gene on the risk of bipolar illness, and the associated marker might represent a proxy for real signals of rare variants.
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findings converge on variation in glutamic acid decarboxylase 1 gene predicting a susceptibility mechanism that affects white matter fractional anisotropy, GABAergic inhibitory neurotransmission in the dorsolateral prefrontal cortex, and working memory performance.
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Results show how epigenetic changes in GAD1 expression alter local glutamate metabolism in the brain metastatic microenvironment, contributing to a metabolic adaption that facilitates metastasis outgrowth in that setting.
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We investigate the possible influence of GAD1 SNPs rs3749034 and rs11542313 on ADHD susceptibility. The C allele of rs11542313 was significantly overtransmitted from parents to ADHD probands. Hyperactive/impulsive score was higher in rs3749034G allele and rs11542313C allele carriers. GAD1 haplotypes were associated with higher hyperactive/impulsive scores in ADHD youths. GAD1 gene is associated with ADHD susceptibility.
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GAD1 is reactivated by DNA methylation, which provided a model for DNA methylation and the active orchestration of oncogenic gene expression by CTCF in cancer cells.
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There was no difference in GAD25 and GAD67 gene expression level, and GAD25/GAD67 ratio between patients with first episode psychosis and healthy controls
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Genetic variability in GAD1 and GAD2 contributes to the risk of methamphetamine dependence in the Thai population.
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Reduced GAD67 expression in PV neurons is not an upstream cause of the lower levels of GABA-associated transcripts, or of the characteristic behaviors, in schizophrenia.
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Glutamic acid decarboxylase 67 (GAD67) is one of the isoforms that catalyze GABA synthesis. Here, we used recombinant herpes simplex virus (HSV-1) vectors that encode gad1 gene to evaluate the therapeutic potential of GAD67 in peripheral HIV gp120-induced neuropathic pain
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This study showed that in female groups, the expression of GABRA5 was generally higher in schizophrenia cases compared to the control.
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GAD autoantibodies were associated with risk of developing type 1 diabetes.
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Conversion of GAD autoantibody is associated with patients with presumed type 2 diabetes.
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The GAD65-independent mechanism for targeting of GAD67 to synaptic vesicles in neurons is not functional in islet beta-cells.
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These results suggest a link between altered inhibitory mechanisms and synchrony and, therefore point to potential mechanisms via which a disruption in neurodevelopmental processes might lead to pathophysiology associated with schizophrenia.
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Gene ransfer of GAD67 by herpes simplex virus vectors prevents HIV gp120/ddC-induced neuropathic pain.
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Phosphate-activated glutaminase and GAD65/67 concentrations are compared in Alzheimer's disease cerebellum versus normal cerebellum controls