Association study of the adrenergic receptors and childhood‐onset mood disorders in Hungarian families

Burcescu, Irina; Wigg, Karen; Gomez, Lissette; King, Nicole; Vetró, Ágnes; Kiss, É; Kapornai, Krisztina; Gádoros, Júlia; Kennedy, James L.; Kovács, Mária; Barr, Cathy L.

doi:10.1002/ajmg.b.30292

Cited by 16 publications

(11 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These assessments were reviewed by two independent child psychiatrists trained in best‐estimate diagnosis who together arrived at a consensus diagnosis. The recruitment and assessment of this sample are described in more detail elsewhere (Burcescu et al. , 2006; Liu et al.…”

Section: Methodsmentioning

confidence: 99%

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

Dempster

Burcescu

Wigg

et al. 2009

Eur J of Neuroscience

View full text Add to dashboard Cite

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.

show abstract

Section: Methodsmentioning

confidence: 99%

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

Dempster

Burcescu

Wigg

et al. 2009

Eur J of Neuroscience

View full text Add to dashboard Cite

show abstract

“…β 1 AR was mapped on chromosome 10q24-q26. Studies have manifested a relationship between this region and depressive disorders (20,21). All β _________________________________________ receptor subtypes couple to the stimulatory Gprotein (Gs) therefore activate the cyclic adenosine monophosphate (cAMP) signalling.…”

Section: Introductionmentioning

confidence: 99%

Beta Adrenoceptor Polymorphism and Clinical Response to Sertraline in Major Depressive Patients

et al. 2017

View full text Add to dashboard Cite

-Purpose: The adrenoceptor family, as one of the main contributors in regulating the noradrenergic system, has been studied in involvement of depression and its treatment. A functional polymorphism of G1165C on beta adrenoceptor (βAR) enhances post receptor signalling and is assumed to be involved in pharmacotherapy of depression. The aim of the present study was to discern the influence of G1165C polymorphism in the β1AR gene on individual differences in response to sertraline. Methods: One hundred newly diagnosed patients completed 6 weeks of sertraline treatment. Response to treatment was defined as a 50% decrease in Hamilton Rating Scale for depression (HRSD). Results: The patients who carried CC genotype responded five times more to sertraline comparing with other variants (P=0.005; OR=5.7; 95%CI=1.4-23.9). Moreover, carriers of C allele responded three times more to sertraline than patients with the G allele (P=0.001; OR= 3.3; 95%CI= 1.72-6.50). Conclusion:In conclusion, our results support the hypothesis that genetic variation of β1AR might influence clinical response to sertraline.

show abstract

“…Conversely, we did not find significant associations between the two ADRA2A variants and GAD or phobia. A number of prior studies have examined the associations between ADRA2A variants and depression or schizophrenia but they also failed to find significant associations 27 54 55 56 .…”

Section: Discussionmentioning

confidence: 99%

Preliminary evidence for a role of the adrenergic nervous system in generalized anxiety disorder

Zhang

Norton

Carrière

et al. 2017

Sci Rep

View full text Add to dashboard Cite

Generalized anxiety disorder (GAD) is a common chronic condition that is understudied compared to other psychiatric disorders. An altered adrenergic function has been reported in GAD, however direct evidence for genetic susceptibility is missing. This study evaluated the associations of gene variants in adrenergic receptors (ADRs) with GAD, with the involvement of stressful events. Data were obtained from 844 French community-dwelling elderly aged 65 or over. Anxiety disorders were assessed using the Mini-International Neuropsychiatry Interview, according to DSM-IV criteria. Eight single-nucleotide polymorphisms (SNPs) involved with adrenergic function were genotyped; adrenergic receptors alpha(1A) (ADRA1A), alpha(2A) (ADRA2A), and beta2 (ADRB2) and transcription factor TCF7L2. Questionnaires evaluated recent stressful life events as well as early environment during childhood and adolescence. Using multivariate logistic regression analyses four SNPs were significantly associated with GAD. A 4-fold modified risk was found with ADRA1A rs17426222 and rs573514, and ADRB2 rs1042713 which remained significant after Bonferroni correction. Certain variants may moderate the effect of adverse life events on the risk of GAD. Replication in larger samples is needed due to the small case number. This is the first study showing that ADR variants are susceptibility factors for GAD, further highlighting the critical role of the adrenergic nervous system in this disorder.

show abstract

Association study of the adrenergic receptors and childhood‐onset mood disorders in Hungarian families

Cited by 16 publications

References 26 publications

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

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

Beta Adrenoceptor Polymorphism and Clinical Response to Sertraline in Major Depressive Patients

Preliminary evidence for a role of the adrenergic nervous system in generalized anxiety disorder

Contact Info

Product

Resources

About