|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
CTD_human |
Alterations in schizophrenia included decreased GAD1 expression and H3K4-trimethylation, predominantly in females and in conjunction with a risk haplotype at the 5' end of GAD1.
|
17942719 |
2007 |
|
Schizophrenia
|
0.400 |
GeneticVariation
|
disease |
LHGDN |
These findings suggest that the GABRB2 and GAD1 genes alone and the combined effects of the polymorphisms in the four GABAergic system genes may confer susceptibility to the development of schizophrenia in the Chinese population.
|
17412563 |
2007 |
|
Schizophrenia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
These findings suggest that the GABRB2 and GAD1 genes alone and the combined effects of the polymorphisms in the four GABAergic system genes may confer susceptibility to the development of schizophrenia in the Chinese population.
|
17412563 |
2007 |
|
Schizophrenia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Alterations in schizophrenia included decreased GAD1 expression and H3K4-trimethylation, predominantly in females and in conjunction with a risk haplotype at the 5' end of GAD1.
|
17942719 |
2007 |
|
Schizophrenia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The mRNA expression level of an epigenetically regulated schizophrenia candidate gene GAD67 was strongly and negatively correlated with the mRNA expression levels of HDAC1, HDAC3 and HDAC4 levels.
|
17961987 |
2008 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
We found that the density of GAD67+ neurons in layers 2-5 of the prefrontal cortex was decreased by 27-36% in both schizophrenia and bipolar disorder.
|
18534564 |
2008 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
CTD_human |
Schizophrenia subjects showed significant decreases in mRNA levels of GAD(67), GAD(65), GAT-1, mGluR2, and neuronal nitric oxide synthase.
|
18923069 |
2008 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
(i) In animal models, NMDAR antagonists reduce parvalbumin and GAD67, as found in schizophrenia.
|
18395805 |
2008 |
|
Schizophrenia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Given that the switch from G to T in SNP rs3791878 might cause the loss of ARNT and XBP1 transcriptional factor binding sites using a bioinformatics approach, our positive findings of this SNP support the hypothesis that the abruption of GAD1 gene is important to the risk of schizophrenia.
|
18335162 |
2008 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
LHGDN |
Given that the switch from G to T in SNP rs3791878 might cause the loss of ARNT and XBP1 transcriptional factor binding sites using a bioinformatics approach, our positive findings of this SNP support the hypothesis that the abruption of GAD1 gene is important to the risk of schizophrenia.
|
18335162 |
2008 |
|
Schizophrenia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Schizophrenia subjects showed significant decreases in mRNA levels of GAD(67), GAD(65), GAT-1, mGluR2, and neuronal nitric oxide synthase.
|
18923069 |
2008 |
|
Schizophrenia
|
0.400 |
AlteredExpression
|
disease |
LHGDN |
Subjects with schizophrenia exhibited expression deficits in GABA-related transcripts encoding (1) presynaptic regulators of GABA neurotransmission (67 kDa isoform of glutamic acid decarboxylase (GAD(67)) and GABA transporter 1), (2) neuropeptides (somatostatin (SST), neuropeptide Y (NPY) and cholecystokinin (CCK)) and (3) GABA(A) receptor subunits (alpha1, alpha4, beta3, gamma2 and delta).
|
17471287 |
2008 |
|
Schizophrenia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Subjects with schizophrenia exhibited expression deficits in GABA-related transcripts encoding (1) presynaptic regulators of GABA neurotransmission (67 kDa isoform of glutamic acid decarboxylase (GAD(67)) and GABA transporter 1), (2) neuropeptides (somatostatin (SST), neuropeptide Y (NPY) and cholecystokinin (CCK)) and (3) GABA(A) receptor subunits (alpha1, alpha4, beta3, gamma2 and delta).
|
17471287 |
2008 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
CTD_human |
This remodeling might contribute to reelin- and GAD(67)-promoter demethylation and might reverse the GABAergic-gene-expression downregulation associated with SZ morbidity.
|
19110320 |
2009 |
|
Schizophrenia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In the second approach, we measured GAD67 mRNA and total H3K9,K14ac levels in lymphocytes from 11 schizophrenia and 7 bipolar patients before and after 4 weeks of clinical treatment with Depakote ER (VPA).
|
19187942 |
2009 |
|
Schizophrenia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
This molecular remodeling may contribute to the induction of reelin (RELN) and GAD(67) (GAD1) promoter demethylation, and may reverse the downregulation of various GABAergic mRNAs and proteins detected in the telencephalon of patients with schizophrenia or bipolar disorders.
|
22122643 |
2009 |
|
Schizophrenia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
This remodeling might contribute to reelin- and GAD(67)-promoter demethylation and might reverse the GABAergic-gene-expression downregulation associated with SZ morbidity.
|
19110320 |
2009 |
|
Schizophrenia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In addition, neuropeptide Y (NPY), which is a phenotypic marker of a sub-population of GAD1-containing interneurons, has shown reduced expression in the prefrontal cortex in subjects with schizophrenia, suggesting that dysfunction of the NPY+ cortical interneuronal sub-population might be a core feature of this devastating disorder.
|
20125089 |
2010 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Our findings confirm that GABA deficits (reduced GAD67) are a consistent feature of schizophrenia postmortem brain studies.
|
20100621 |
2010 |
|
Schizophrenia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
We also examined whether a schizophrenia risk-associated promoter SNP in GAD1 (rs3749034) is related to expression of these transcripts.
|
21795557 |
2011 |
|
Schizophrenia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The findings that lower GAD67 mRNA expression is common in schizophrenia, that it is not a consequence of having the illness, and that it leads to less translation of the protein, especially in the axon terminals of parvalbumin-containing neurons, support the hypothesis that lower GABA synthesis in parvalbumin neurons contributes to dorsolateral prefrontal cortex dysfunction and impaired cognition in schizophrenia.
|
21632647 |
2011 |
|
Schizophrenia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In addition, GAD67 mRNA levels were reduced in patients with schizophrenia in both the DG (23%) and CA4 (60%) compared with controls.
|
21223646 |
2011 |
|
Schizophrenia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The expression of AK098371 is associated with a GAD1 single nucleotide polymorphism (rs3749034) that previously has been associated with GAD67 expression and risk for schizophrenia.
|
22496567 |
2012 |
|
Schizophrenia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The findings that reduced GAD(67) mRNA expression can induce lower CB1R mRNA expression support the hypothesis that lower cortical levels of CB1Rs in schizophrenia may partially compensate for deficient GAD(67)-mediated GABA synthesis by reducing endogenous cannabinoid suppression of GABA release.
|
22036037 |
2012 |
|
Schizophrenia
|
0.400 |
Biomarker
|
disease |
BEFREE |
The copy number intensities examined using both microarrays and quantitative real-time polymerase chain reaction for the GAD67 gene were significantly decreased in sector CA3/2 of patients with schizophrenia and patients with bipolar disorder.
|
22309971 |
2012 |