Although we did not replicate the specific interaction of abuse and the TAT-haplotype of the CRHR1 gene we confirmed the relevance of an interplay between variants within the CRHR1 gene and childhood adversities in the modulation of depression in adults.
Growth curve models were executed to determine whether CRHR1 moderated the link between Wave 1 family economic hardship and youths' development of depression.
Single nucleotide polymorphisms in the CRH receptor 1 (CRHR1) gene interact with ELS to predict depression, cognitive functions and hippocampal activity.
Several studies have demonstrated that variants of the CRH-R1 gene carry a potential risk for depression, but evidence for an association between CRH-R1 genotypes and IBS is lacking.
Previous research supports gene-environment interactions for polymorphisms in the corticotropin hormone receptor 1 gene (CRHR1) and the serotonin transporter gene linked polymorphic region (5-HTTLPR) in predicting depression, but it has rarely considered genetic influences on stress sensitization processes, whereby early adversities (EA) increase depressive reactivity to proximal stressors later in life.
These data demonstrate that the CRHR1 TAT haplotype is associated with cognitive features of depression including difficulty with decision-making, higher rumination, and poorer learning and memory.
Corticotropin-releasing factor receptor type 1 (CRF1R) is a class B receptor mediating stress response and also considered a drug target for depression and anxiety.
To replicate the interaction between childhood maltreatment and a TAT haplotype formed by rs7209436, rs110402, and rs242924 in CRHR1, predicting adult depression.
In addition, GR and corticotropin-releasing hormone receptor 1 (CRHR1) genotypes contributed significantly to psychosis measures and CRHR1 contributed significantly to depression severity rating.
When all subjects were grouped based on family history of mental illness, there was a statistically significant association of CRHR1rs242941 with family history regardless of depression status (P = 0.043).
Dysregulation in the stress response of the hypothalamic-pituitary-adrenocortical (HPA) axis, involving the corticotrophin-releasing hormone (CRH) and its main receptor (CRHR1), is associated with depression, frequent among suicidal males.
The complex structure of CRHR1 may help to explain why some variants in the gene moderate the effects of an ACE only on depression risk while others moderate the effect of an ACE only on AD risk.
Corticotropin-releasing factor binds with high affinity to CRF receptor 1 (CRFR1) and is implicated in stress-related mood disorders such as anxiety and depression.
The present study partially replicates recent findings of a CRHR1 by childhood adversity interaction with regard to adult depression highlighting the subjective characteristics of the environmental pathogen that is operative in this interaction.
EA treatment can decrease the expression of hypothalamic CRF and CRF-R1, relieve anxiety and depression, meanwhile reduce the expression of CRF-R1 in the gastrointestinal mucosa, increase ZO-1 expression, and adjust tight junctions (TJs) to repair the intestinal mucosal barrier.
The analysed candidate haplotypes in FKBP5, NR3C1, and CRHR1 did not show an association with depression scores as assessed by EPDS in this cohort of healthy unselected pregnant women.
This study was conducted to determine whether CRHR1 polymorphisms interact with childhood maltreatment to predict hypothalamic-pituitary-adrenal (HPA) axis reactivity, which has been linked to both depression and early life stress.
Similarly, we recently discovered that genetic variation in components of the stress-related hypothalamic pituitary adrenocortical axis, T-box 19 and corticotropin releasing hormone receptor 1, showed association and linkage to high anger/hostility in and male depression the suicidal offspring, respectively.
The recent characterisation of several selective small-molecule CRHR1 antagonists offers new possibilities for the treatment of anxiety and depression.
In the present study, we demonstrated that chronic FS stress (CFSS) could activate corticotropin-releasing factor (CRF)/CRF receptor type 1 (CRFR1) signaling in the BLA, and blockade of CRF/CRFR1 signaling by intra-BLA injection of NBI27914 (NBI), a selective CRFR1 antagonist, could prevent the CFSS-induced depressive-like behaviors in rats, indicating that activation of CRF/CRFR1 signaling in the BLA is required for CFSS-induced depression.
Stress and anxiety disorders are risk factors for depression and these behaviors are modulated by corticotrophin-releasing factor receptor 1 (CRFR1) and serotonin receptor (5-HT(2)R).
Depression and anxiety symptoms among women who carry the FMR1 premutation: impact of raising a child with fragile X syndrome is moderated by CRHR1 polymorphisms.