Regression analyses indicated that patients with the A/A genotype for the IL-10 -1082 polymorphism (lower IL-10 producers) reported significantly greater depressive symptoms than G allele carriers (higher IL-10 producers; b = 0.22, P = 0.011), even after controlling for relevant covariates.
There were significant interactions between SULT1A1*3 and hot flashes (P < 0.001) and between SULT1A1*2 and depressive symptoms (P = 0.007) on menopausal stage, and there were race-specific effects of SULT1A1*2, SULT1A1*3, CYP1B1*3, and CYP3A4*1B on menopause.
Previous studies have revealed the association of the ACE gene insertion/deletion polymorphism with depressive disorder and its treatment response but not with the depressive symptoms in schizophrenia.
Taken together, these findings indicate that sensitivity of p38 MAPK signaling pathways to immune stimulation is associated with depressive symptoms during chronic IFN-alpha treatment.
Our preliminary results suggest that the SERPINE1 promoter polymorphisms may be associated with antidepressant treatment, but not with the increased susceptibility to the depressive symptoms in AD.
In Japanese women, the odds of depressive symptoms were nearly 5-fold higher among those with CYP 19 rs936306 TT genotype (95% CI, 1.10 to 22.17) than in women with the CC genotype and 9.6-fold higher (95% CI, 2.01 to 45.81) than in women with the CT genotype.
No SNPs were associated with the personality and psychological distress traits at a Bonferroni corrected level of significance (P < 0.0002), but there was an over-representation of nominally significant (P < 0.05) SNPs in the synaptojanin-2 (SYNJ2) gene associated with agreeableness and symptoms of depression.
These data suggest a potential role for DAO in susceptibility to depressive symptoms in schizophrenia, but a more general role for DAO in affective disorders cannot be excluded.
In conclusion, our results show that genetic variance in the VDR gene influences the susceptibility to age-related changes in cognitive functioning and in depressive symptoms.
Among Caucasian women, those with the CYP1A1 rs2606345 CC and AC genotypes had approximately 2-fold greater odds of having depressive symptoms than did those with the AA genotype (95% confidence intervals [CIs], 1.33 to 4.66 and 1.25 to 3.14, respectively).
There were significant interactions between SULT1A1*3 and hot flashes (P < 0.001) and between SULT1A1*2 and depressive symptoms (P = 0.007) on menopausal stage, and there were race-specific effects of SULT1A1*2, SULT1A1*3, CYP1B1*3, and CYP3A4*1B on menopause.
Our previous work has shown genetic variation in the human choline transporter gene (CHT1) to be associated with depressive symptoms and autonomic cardiac (cholinergic) dysregulation.
There was moderate statistical evidence for interactions for other shoulder pain phenotypes between additional genes (ADRB2, AVPR1 A, and KCNS1) and depressive symptoms, pain catastrophizing, or kinesiophobia.
An association between symptoms of depression and rs7582472 (near to MGAT5 and NCKAP5) was replicated in two independent samples, but other replication findings were less consistent.
To define better this neuropsychiatric phenotype associated with premutation carriers and to minimize a possible environmental effect, we examined psychiatric and depressive symptoms in 34 FMR1 premutation carrier mothers of children with fragile-X syndrome in comparison with two control groups (39 mothers with a non-fragile-X syndrome mentally retarded child and 39 mothers from the general population).
Our studies indicate that the AVP and its V1b receptor system may be a potential therapeutic target for treating anxiety and depressive symptoms associated with cocaine addiction.
This preliminary result suggests that the promoter GT repeat dinucleotide microsatellite polymorphism of the IFNAR1 gene may represent a risk factor for the development of depressive symptoms during IFN-alpha therapy for hepatitis C and other conditions.
To evaluate ApoE alleles in relation to symptoms of depression in a cohort of patients with MS participating in the Sonya Slifka Longitudinal Multiple Sclerosis Study (Slifka Study).
Namely, R3HDML and C20orf39 are significantly associated with depressive symptoms of schizophrenia (P(emp)<2×10⁻⁵) based on the minimum P-value and truncated-product methods, respectively.