Mood Disorder Patients (mood + disorder_patient)

Distribution by Scientific Domains

Selected Abstracts

Further genetic evidence implicates the vasopressin system in childhood-onset mood disorders

Emma L. Dempster
Abstract Studies in both animals and humans advocate a role for the vasopressin (AVP) system in the aetiology of depressive symptoms. Attention has particularly focused on the role of AVP in the overactivation of the hypothalamic-pituitary-adrenal (HPA)-axis in mood disorders. Elevated AVP plasma levels have been found in mood disorder patients, which are often positively correlated with the severity of symptoms. We recently reported an association between childhood-onset mood disorders (COMD) and polymorphisms in the receptor responsible for the AVP-mediated activation of the HPA-axis (AVPR1B). As genetic variation in the vasopressinergic system could provide a mechanism to explain the endocrine alterations observed in mood disorders, we investigated other genes in this system. The gene encoding AVP is the strongest candidate, particularly as genetic variation in this gene in rodents is associated with anxiety-related behaviours. Six single-nucleotide polymorphisms (SNPs) were genotyped across the AVP gene in a sample comprised of 586 Hungarian nuclear families ascertained through affected probands with a diagnosis of COMD. In addition, AVP coding and putative regulatory regions were screened for mutations using denaturing high-performance liquid chromatography. One SNP, 3, to the AVP, gene reached significance (P = 0.03), as did the overtransmission of a five-marker haplotype with a frequency of 22% (P = 0.0001). The subsequent mutation screen failed to identify any putative functional polymorphisms. The outcome of this study, combined with our previous association between COMD and AVPR1B, implicates genetic variation in vasopressinergic genes in mediating vulnerability to COMD. [source]

Association study between cannabinoid receptor gene (CNR1) and pathogenesis and psychotic symptoms of mood disorders,

Shih-Jen Tsai MD
Abstract Cannabis can induce mood change and sometimes psychotic symptoms in normal persons. In brain, the main active ingredient of cannabis acts via the cannabinoid CB1 receptor (CNR1) which is located on chromosome 6q14-15. Linkage studies have suggested the presence of a bipolar disorder susceptibility locus on chromosome 6q. In this population based association study, we tested the hypothesis that a microsatellite polymorphism in the promoter region of the CNR1 gene confers susceptibility to mood disorders and psychotic features. We genotyped the CNR1 gene is 154 mood disorder patients and 165 normal controls. The results showed that the triplet repeat polymorphism in the promoter region of the CNR1 gene was not likely to be involved in the pathogenesis or in the psychotic symptoms of mood disorders. 2001 Wiley-Liss, Inc. [source]

Improvement of cognitive functioning in mood disorder patients with depressive symptomatic recovery during treatment: An exploratory analysis

Abstract, Depressive symptoms have a large impact on cognitive test performance of mood disorder patients. After remission, some improvement of cognitive functioning has been observed, but also stable deficits have been reported both during depression and remission. In the present study, the authors aimed to investigate the cognitive functioning of mood disorder patients in relation to early symptomatic recovery, by comparing performances at the Wechsler Adult Intelligence Scale-Revised (WAIS-R) of responders and non-responders to the antidepressant treatment. The sample was composed of 51 hospitalized patients for a major depressive episode (major depressives/bipolars = 37/14). All patients were treated with fluvoxamine and evaluated at baseline and after 4 weeks using the 21-item Hamilton Rating Scale for Depression. All subjects were once assessed for their cognitive functioning with the WAIS-R, at the end of the fourth week of treatment. In the current sample, patients who showed a significant symptomatic remission after 4 weeks of treatment showed higher total WAIS-R scores and a lower incidence of cognitive impairment, compared to non-responders to treatment. No major differences could be observed on any particular subtest, but rather a global improving of scores in responders compared to non-responders to pharmacotherapy. Pre-treatment illness severity, that was significantly higher among non-responders, was significantly associated with patients' intelligence quotient scores. Despite a number of limitations, present data support a strong effect of depressive symptoms on patients WAIS-R performances and an early global improvement of cognitive functioning concurrent with symptomathology recovery during pharmacological treatment. [source]