Clinical and Genetic Dissection of Anger Expression and CREB1 Polymorphisms in Major Depressive Disorder

Perlis, Roy H.; Purcell, Shaun; Fagerness, Jesen; Cusin, Cristina; Yamaki, Lesley H.; Fava, Maurizio; Smoller, Jordan W.

doi:10.1016/j.biopsych.2006.10.034

Cited by 42 publications

(43 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The interaction of sex with CREB1 variants that influence the development of psychiatric syndromes, or their clinical features, seems likely to be complex and allele specific. As an example, Perlis et al 37,38 have recently described associations of non-coding SNPs in the CREB1 region with expressed anger and treatment-emergent suicidal ideation among men with MDD that are less evident or absent among women with this disorder. Whether these genotypes affect the risk of developing syndromic MDD among men or women cannot be determined from these studies.…”

Section: Discussionmentioning

confidence: 99%

Effects of the G(−656)A variant on CREB1 promoter activity in a neuronal cell line: Interactions with gonadal steroids and stress

Zubenko

Hughes

2008

Mol Psychiatry

View full text Add to dashboard Cite

Major depressive disorder (MDD) constitutes a major public health problem worldwide and affects women twice as frequently as men. Previous genetic studies have revealed significant evidence of linkage of the cAMP-responsive element-binding protein 1 (CREB1) gene region (2q33-35) to mood disorders among women from families with recurrent, early-onset MDD (RE-MDD), a severe and familial subtype of MDD. A rare G-to-A transition at position À656 in the CREB1 promoter co-segregates with mood disorders in women from these families, implicating CREB1 as a sex-related susceptibility gene for unipolar mood disorders. In the current study, the functional significance of the CREB1 promoter variant was determined using transfection experiments that employed plasmid constructs containing the wild-type or variant CREB1 promoters coupled to a reporter gene. The results support the hypothesis that the A À656 allele contributes to the development of MDD in women through selective alteration of CREB1 promoter activity by female gonadal steroids in noradrenergic neuronal cells. Furthermore, exaggeration of these effects during a simulated stress condition may be relevant to reported gene-environment interactions that contribute to the emergence of MDD in clinical populations.

show abstract

Section: Discussionmentioning

confidence: 99%

Effects of the G(−656)A variant on CREB1 promoter activity in a neuronal cell line: Interactions with gonadal steroids and stress

Zubenko

Hughes

2008

Mol Psychiatry

View full text Add to dashboard Cite

show abstract

“…11) In other papers, Perlis et al reported that T allele in rs4675690 was associated with greater internal effort at anger control, greater risk of treatment-emergent suicidal ideation in MDD. 5,6) There were reports that depressed patients are significantly greater levels of anger than normal controls 12) and anger attacks are improved by antidepressant treatment. 13) Anger might overlap only partially with their effects on depression.…”

Section: Resultsmentioning

confidence: 99%

“…CREB1 was reported that the association with neuronal signal transduction involved in synaptic plasticity 2) and antidepressant response. 3,4) In Caucasian population, CREB1 rs4675690 polymorphism was associated with anger expression in male MDD patients 5) and suicidal behaivor in MDD patients. 6) While PCLO was localized in the presynaptic active zone 7) and involved in monoamine neurotransmission.…”

mentioning

confidence: 97%

Genotype Distributions and Allele Frequencies of Possible Major Depressive Disorder-Associated Single Nucleotide Polymorphisms, Cyclic Adenosine Monophosphate Response Element Binding Protein 1 rs4675690 and Piccolo rs2522833, in a Japanese Population

Inoue

Ando

Suzuki

et al. 2012

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

It is known that the onset of major depressive disorder (MDD) would be associated with genetic factors. To investigate the susceptibility to psychiatric disorders, e.g. MDD, schizophrenia etc., it is necessary to compare the genetic differences of objective polymorphisms between in patients and in relative contol subjects. Recently, an increasing number of studies focused on the role of cyclic adenosine monophosphate response element binding protein 1 (CREB1) and Piccolo (PCLO) on MDD. However, there was no report about genetic characterization of polymorphisms in between MDD patients and healthy subjects in Japanese population. We analized genotype distributions and allele frequencies of CREB1 rs4675690 and PCLO rs2522833 polymorphisms in 267 Japanese subjects, respectively. In CREB1 rs4675690, C allele frequency (0.41) was lower than T allele (0.59). While in PCLO rs2522833, A allele frequency (0.45) was lower than C allele (0.55). Our findings may be useful for investigating the genetic factors concerning the susceptibility to MDD in Japanese population.Key words cAMP response element binding protein 1; Piccolo; polymorphism; Japanese; major depressive disorder Major depressive disorder (MDD) is a familial disorder and its familiarity mostly or entirely results from genetic influence.1) To investigate disease susceptibility affected by genetic polymorphism, it is often performed with comparison of genotype distributions and allele frequencies of objective polymorphism in patients with in its relative control subjects.Recently, an increasing number of studies focused on the role of transcription factor, cyclic adenosine monophosphate response element binding protein 1 (CREB1) and presynaptic cytomatrix protein, Piccolo (PCLO) on MDD. CREB1 was reported that the association with neuronal signal transduction involved in synaptic plasticity 2) and antidepressant response. 3,4) In Caucasian population, CREB1 rs4675690 polymorphism was associated with anger expression in male MDD patients 5) and suicidal behaivor in MDD patients. 6) While PCLO was localized in the presynaptic active zone 7) and involved in monoamine neurotransmission.8) PCLO polymorphism rs2522833 was related with hypothalamic-pituitary-adrenocortical (HPA) regulation during antidepressant treatment and the susceptibility to MDD in Caucasian population. 9)It was suggested that these polymorphisms may be associated with the susceptibility to MDD and therapeutic efficacy of antidepressants in Japanese population. However there was no report about CREB1 rs4675690 and PCLO rs2522833 polymorphisms in Japanese population. In this study, we examined genotype distributions and allele frequencies of CREB1 rs4675690 and PCLO rs2522833 polymorphisms in 267 Japanese healthy subjects. MATERIALS AND METHODS Japanese SubjectsThis study was performed in accordance with the Declaration of Helsinki and Good Clinical Practice guidelines, and approved by the Ethics Committee of the University of Shizuoka, Shizuoka, Japan (approved number 18-2). A total of 267 Japanese...

show abstract

“…Perlis et al have also reported that the presence of the rs4675690 T allele of CREB1 is associated with a greater internal effort at anger control and a greater risk of treatmentemergent suicidal ideation in patients with major depressive disorders. 32,33) Depressed patients can also have significantly greater levels of anger compared with normal controls, 34) and bouts of anger can be improved by antidepressant treatment. 35) This effect on anger might partially overlap with the effects on depression.…”

Section: )mentioning

confidence: 99%

Influence of Genetic Polymorphisms and Concomitant Anxiolytic Doses on Antidepressant Maintenance Doses in Japanese Patients with Depression

Inoue

Murofushi

Nagaoka

et al. 2016

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

To prevent recurrent depression, patients should ideally continue treatment for >6 months with the antidepressant dose that effectively suppressed acute depressive symptoms. However, there are inter-individual differences in the antidepressant doses required to achieve response and maintenance. Therefore, this study was conducted to examine the role of clinical features, including genetic polymorphisms, on the antidepressant dose required for maintenance therapy in 82 Japanese patients with depression. We calculated the antidepressant dose using the imipramine equivalent scale and the dose of concomitant anxiolytics and hypnotics using the diazepam equivalent scale. The 82 participants were classified into two groups based on the median imipramine equivalent dose, and we examined the influence of patient characteristics and the presence of genetic polymorphisms of brain-derived neurotropic factor (BDNF; rs6265) and cyclic adenosine monophosphate responsive element-binding protein 1 (CREB1; rs2253306, rs4675690, rs769963) on the antidepressant maintenance dose. Using a multivariate logistic regression analysis, we found that the concomitant diazepam equivalent dose and presence of the CREB1 rs4675690 polymorphism were significantly associated with the antidepressant maintenance dose. We concluded that these factors influenced the antidepressant dose in maintenance therapy among Japanese patients with depression. However, further research is required in large cohorts.Key words antidepressant; maintenance dose; depressive disorder; polymorphism; brain-derived neurotrophic factor; cyclic AMP responsive element binding protein 1 Depressive disorder is a common psychiatric disorder, with approximately 350 million people being affected worldwide. 1)Moreover, it is associated with a high rate of recurrence and chronicity, with 12-35% of all cases becoming chronic and 13.2% experiencing recurrence within 5 years.2-5) When starting antidepressant therapy, the dose of antidepressant is low and is slowly increased, and careful attention is paid to the development of anxiety, agitation, panic attacks, insomnia, irritability, hostility, aggressiveness, impulsivity, akathisia, hypomania, and mania, the so-called "activation syndrome." The target dose is the lowest dose that adequately suppresses depressive symptoms with tolerable side effects. After achieving remission, the therapeutic dose acutely required is continued as maintenance therapy for >6 months to prevent recurrence. 6,7)Several reports suggest that when an antidepressant is ineffective in suppressing depressive symptoms, combination therapy with another antidepressant or anxiolytic or hypnotic drugs is more effective than increasing the dose of the preexisting antidepressant. [8][9][10] In studies on Japanese patients with depression, 23.4-35.9% of cases were treated with antidepressant combination therapy and 60.3-73.0% were treated with concomitant anxiolytic or hypnotic drugs. In addition, it is known that inter-individual differences exist in the daily dosing ...

show abstract

Clinical and Genetic Dissection of Anger Expression and CREB1 Polymorphisms in Major Depressive Disorder

Cited by 42 publications

References 52 publications

Effects of the G(−656)A variant on CREB1 promoter activity in a neuronal cell line: Interactions with gonadal steroids and stress

Effects of the G(−656)A variant on CREB1 promoter activity in a neuronal cell line: Interactions with gonadal steroids and stress

Genotype Distributions and Allele Frequencies of Possible Major Depressive Disorder-Associated Single Nucleotide Polymorphisms, Cyclic Adenosine Monophosphate Response Element Binding Protein 1 rs4675690 and Piccolo rs2522833, in a Japanese Population

Influence of Genetic Polymorphisms and Concomitant Anxiolytic Doses on Antidepressant Maintenance Doses in Japanese Patients with Depression

Contact Info

Product

Resources

About