|
Depressive disorder
|
0.600 |
Biomarker
|
disease |
BEFREE |
The present study shows that depression attenuates the mechanical allodynia and thermal hyperalgesia of neuropathic pain and suggests that altered spinal GR-BDNF-TrkB signaling may be one of the reasons for depression-induced hypoalgesia.
|
28579944 |
2017 |
|
Depressive disorder
|
0.600 |
Biomarker
|
disease |
BEFREE |
FKBP5 and specific microRNAs via glucocorticoid receptor in the basolateral amygdala involved in the susceptibility to depressive disorder in early adolescent stressed rats.
|
28826069 |
2017 |
|
Depressive disorder
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Recent human studies show that DNA methylation changes of hypothesis-driven candidate gene regions, such as the promoter of the glucocorticoid receptor and the serotonin transporter, were associated with maternal depression in peripheral tissue samples of newborns' cord blood, infants' saliva, or adults' peripheral blood.
|
28714605 |
2017 |
|
Depressive disorder
|
0.600 |
Biomarker
|
disease |
BEFREE |
The hypo‑level of adrenocorticotropic hormone, noradrenaline and glucocorticoid receptor in serum and hypothalamus of depression‑like rats was enhanced by PHC.
|
28849191 |
2017 |
|
Depressive disorder
|
0.600 |
Biomarker
|
disease |
BEFREE |
Glucocorticoid receptor gene modulates severity of depression in women with crack cocaine addiction.
|
27397864 |
2016 |
|
Depressive disorder
|
0.600 |
Biomarker
|
disease |
BEFREE |
Epigenetics and the glucocorticoid receptor: A review of the implications in depression.
|
27344028 |
2016 |
|
Depressive disorder
|
0.600 |
Biomarker
|
disease |
BEFREE |
Altered DNA methylation (DNAm) levels of hypothalamic-pituitary-adrenal (HPA) axis genes has been associated with exposure to childhood maltreatment (CM) and depression; however, it is unknown whether CM and depression have joint and potentially interacting effects on the glucocorticoid receptor (NR3C1) DNAm.
|
27475889 |
2016 |
|
Depressive disorder
|
0.600 |
PosttranslationalModification
|
disease |
BEFREE |
In this first study in humans to examine the joint effects of prenatal and postnatal environmental exposures, we report that GR gene (NR3C1) 1-F promoter methylation in infants is elevated in the presence of increased maternal postnatal depression following low prenatal depression, and that this effect is reversed by self-reported stroking of the infants by their mothers over the first weeks of life.
|
25942041 |
2015 |
|
Depressive disorder
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
The externalizing disorders group had significantly lower NR3C1 methylation levels than the lifetime depressive disorder group (p = 0.009) and healthy controls (p = 0.001) This report of lower methylation levels in NR3C1 in externalizing disorders may indicate a mechanism through which the differential development of externalizing disorders as opposed to depressive disorders might occur.
|
25894927 |
2015 |
|
Depressive disorder
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Allelic variants of the glucocorticoid receptor (GR) gene contribute significantly to both cortisol levels and to measures of psychosis; corticotropin-releasing hormone receptor 1 variants contribute to measures of depression and psychosis.
|
24933348 |
2015 |
|
Depressive disorder
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Network modeling and animal experiments suggest that these genetic differences in GR-induced transcriptional activation may mediate the risk for depression and other psychiatric disorders by altering a network of functionally related stress-sensitive genes in blood and brain.
|
26050039 |
2015 |
|
Depressive disorder
|
0.600 |
Biomarker
|
disease |
BEFREE |
The glucocorticoid receptor (GR) gene (NR3C1) has been found to be susceptible to epigenetic modification, specifically DNA methylation, in the context of environmental stress such as early life trauma, which is an established risk for depression later in life.
|
26387521 |
2015 |
|
Depressive disorder
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Depression has been linked to dysfunction of the intracellular response system to corticosteroids at the level of the hippocampus (HC) and prefrontal cortex (PFC) with a notable role of the glucocorticoid receptor (GR) and its co-chaperones (FKBP5 and FKBP4).
|
25666308 |
2015 |
|
Depressive disorder
|
0.600 |
Biomarker
|
disease |
PSYGENET |
Network modeling and animal experiments suggest that these genetic differences in GR-induced transcriptional activation may mediate the risk for depression and other psychiatric disorders by altering a network of functionally related stress-sensitive genes in blood and brain.
|
26050039 |
2015 |
|
Depressive disorder
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
In addition, GR and corticotropin-releasing hormone receptor 1 (CRHR1) genotypes contributed significantly to psychosis measures and CRHR1 contributed significantly to depression severity rating.
|
24166410 |
2014 |
|
Depressive disorder
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Polymorphisms in the FK506 binding protein 5 (FKBP5) gene have been shown to influence glucocorticoid receptor sensitivity, stress response regulation, and depression risk in traumatized subjects, with most consistent findings reported for the functional variant rs1360780.
|
25522420 |
2014 |
|
Depressive disorder
|
0.600 |
Biomarker
|
disease |
PSYGENET |
We investigated PTSD and depression severity, plasma cortisol, GR and mineralocorticoid receptor (MR) levels, and methylation status of NR3C1 and NR3C2 promoter regions in 25 women exposed to the Tutsi genocide during pregnancy and their children, and 25 women from the same ethnicity, pregnant during the same period but not exposed to the genocide, and their children.
|
24690014 |
2014 |
|
Depressive disorder
|
0.600 |
Biomarker
|
disease |
PSYGENET |
Polymorphisms in the FK506 binding protein 5 (FKBP5) gene have been shown to influence glucocorticoid receptor sensitivity, stress response regulation, and depression risk in traumatized subjects, with most consistent findings reported for the functional variant rs1360780.
|
25522420 |
2014 |
|
Depressive disorder
|
0.600 |
Biomarker
|
disease |
BEFREE |
Recent research suggests an important role of FKBP5, a glucocorticoid receptor regulating co-chaperone, in the development of stress-related diseases such as depression and anxiety disorders.
|
24411633 |
2014 |
|
Depressive disorder
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Bcl1 polymorphism of the glucocorticoid receptor gene and treatment response to milnacipran and fluvoxamine in Japanese patients with depression.
|
25358426 |
2014 |
|
Depressive disorder
|
0.600 |
Biomarker
|
disease |
PSYGENET |
Methylation in CpG sites in candidate genes were not predictors of depression at significance levels corrected for whole genome testing, but maltreated and control children did have significantly different β values after Bonferroni correction at multiple methylation sites in these candidate genes (e.g., BDNF, NR3C1, FKBP5).
|
24655651 |
2014 |
|
Depressive disorder
|
0.600 |
PosttranslationalModification
|
disease |
BEFREE |
We investigated PTSD and depression severity, plasma cortisol, GR and mineralocorticoid receptor (MR) levels, and methylation status of NR3C1 and NR3C2 promoter regions in 25 women exposed to the Tutsi genocide during pregnancy and their children, and 25 women from the same ethnicity, pregnant during the same period but not exposed to the genocide, and their children.
|
24690014 |
2014 |
|
Depressive disorder
|
0.600 |
Biomarker
|
disease |
PSYGENET |
Bcl1 polymorphism of the glucocorticoid receptor gene and treatment response to milnacipran and fluvoxamine in Japanese patients with depression.
|
25358426 |
2014 |
|
Depressive disorder
|
0.600 |
Biomarker
|
disease |
BEFREE |
In this study, we tested the leukocyte mRNA expression levels of genes belonging to glucocorticoid receptor (GR) function (FKBP-4, FKBP-5, and GR), inflammation (interleukin (IL)-1α, IL-1β, IL-4, IL-6, IL-7, IL-8, IL-10, macrophage inhibiting factor (MIF), and tumor necrosis factor (TNF)-α), and neuroplasticity (brain-derived neurotrophic factor (BDNF), p11 and VGF), in healthy controls (n=34) and depressed patients (n=74), before and after 8 weeks of treatment with escitalopram or nortriptyline, as part of the Genome-based Therapeutic Drugs for Depression study.
|
22990943 |
2013 |
|
Depressive disorder
|
0.600 |
PosttranslationalModification
|
disease |
BEFREE |
Conclusively: (1) depression in females may result from a gene × childhood-adversity interaction and/or a dysregulated epigenetic programming of MAOA; (2) childhood-adversity subtypes may differentially impact DNA methylation at NR3C1; (3) baseline MAOA-genotypic variations may affect the extent of NR3C1 methylation.
|
23449091 |
2013 |