<b>Background</b>Although there are consistent reports of higher psychosis rates among immigrants, the information on mood disorders is limited.<b>Aims</b>To review and quantify the difference in incidence of mood disorders in first- and second-generation immigrant (FGI and SGI) groups <i>v.</i> non-immigrants.<b>Method</b>PubMed, EMBASE and PsycINFO were searched for articles from cohort studies reporting incidence of mood disorders among FGIs and SGIs.<b>Results</b>Eighteen studies met our inclusion criteria.
<b>Background</b>Although there are consistent reports of higher psychosis rates among immigrants, the information on mood disorders is limited.<b>Aims</b>To review and quantify the difference in incidence of mood disorders in first- and second-generation immigrant (FGI and SGI) groups <i>v.</i> non-immigrants.<b>Method</b>PubMed, EMBASE and PsycINFO were searched for articles from cohort studies reporting incidence of mood disorders among FGIs and SGIs.<b>Results</b>Eighteen studies met our inclusion criteria.
<b>Conclusions:</b> Although the exact mechanisms in the family remain to be elucidated, our data strongly indicate a probable role of the variant, rs78809014, in the regulatory process of the expression of MAPKAP1 and thus in the development of mood disorder in familial mood disorder.
<b>Conclusions:</b> These findings of genotype-dependent cognitive enhancement across clinical groups support the potential clinical use of the GluK4 deletion allele in personalised medicine strategies and provide new insight into the relationship between genetic variation and mood disorders.
<b>Conclusions:</b> We hypothesise that lowered PON1 total and CMPAase activities may play a role in the pathophysiology of MDs by lowering antioxidant defences thereby increasing the risk of lipid peroxidation and inflammation; lowered inhibition of quorum-sensing lactones thereby increasing bacterial proliferation; and attenuated homocysteine thiolactone catabolism which may trigger immune-inflammatory response and/or induce neurotoxicity.
(1996) found that the frequency of the low-activity short variant (s) of the 5-HTT-linked polymorphic region (5-HTTLPR) was higher among patients with affective disorders than in normal controls.
Mood disorder subjects (N=191) and healthy volunteers (N=125), all Caucasian subjects of European origin, were genotyped for the triallelic 5-HTTLPR polymorphism (higher expressing allele: L(A); lower expressing alleles: L(G), S).
Mood Disorders Diagnosis and Patient Registration Form (SCIP-TURK), Mood Disorder Questionnaire (MDQ), and Hypomania Checklist-32-Revised (HCL-32-R) were applied to all patients by experienced clinicians, and clinical diagnoses were confirmed using Structured Clinical Interview for <i>DSM-IV</i> Axis I Disorders (SCID-I).
Prodynorphin, the precursor of the dynorphin opioid peptides, has been shown to play an important role in several aspects of human diseases and complex traits, e.g., drug abuse, epilepsy, and mood disorders.
Prodynorphin, the precursor of the dynorphin opioid peptides, has been shown to play an important role in several aspects of human diseases and complex traits, e.g., drug abuse, epilepsy, and mood disorders.
Prodynorphin and kappa opioid receptor mRNA expression in the cingulate and prefrontal cortices of subjects diagnosed with schizophrenia or affective disorders.
Prodynorphin and kappa opioid receptor mRNA expression in the cingulate and prefrontal cortices of subjects diagnosed with schizophrenia or affective disorders.
Corticotropin-releasing hormone receptor-2 (CRHR2)-deficient mice display a stress-sensitive and anxiety-like phenotype suggesting that the CRHR2 is a plausible functional candidate gene influencing the reactivity of the HPA axis and therefore the liability to develop affective disorders.
Corticotropin-releasing hormone receptor-2 (CRHR2)-deficient mice display a stress-sensitive and anxiety-like phenotype suggesting that the CRHR2 is a plausible functional candidate gene influencing the reactivity of the HPA axis and therefore the liability to develop affective disorders.
Brain-derived neurotrophic factor (BDNF) has been implicated in the pathogenesis of mood disorders, and the aim of the present study was to test for the presence of linkage disequilibrium between two polymorphisms in the BDNF gene and BP in 283 nuclear families.
Dysbindin is widely expressed in the human brain and binds to the dystrophin-associated protein complex (DPC) which appears to be involved in signal transduction pathways, which have been repeatedly investigated and described as altered or disturbed in affective disorders [McLeod et al.
Dysbindin is widely expressed in the human brain and binds to the dystrophin-associated protein complex (DPC) which appears to be involved in signal transduction pathways, which have been repeatedly investigated and described as altered or disturbed in affective disorders [McLeod et al.