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1
CRY1 Variations Impacts on the Depressive Relapse Rate in a Sample of Bipolar Patients

Antonio Drago,Barbara Monti,Diana De Ronchi,Alessandro Serretti 대한신경정신의학회 2015 PSYCHIATRY INVESTIGATION Vol.12 No.1
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  KCI
  
  스콜라
ObjectiveaaA relevant part of the social and personal burden caused by Bipolar Disorder (BD) is related to depressive phases. Authors investigated the genetic impact of a set of variations located in CRY1, a gene involved in the control of the circadian rhythms, towards depressive episodes in a sample of bipolar patients from the STEP-BD sample. As a secondary analysis, CYR1 variations were analyzed as predictors of sleep disruption. Methodsaa654 bipolar patients were included in the analysis. Data were available genome-wide. The part of the genome coding for the CRY1 was imputed and pruned according to standards in the field. 7 SNPs were available for the analysis. A correction for multitesting was applied and we had sufficient power (0.80) to detect a small-medium effect size (0.22) between two allelic frequencies each one represented by at least 300 subjects. ResultsaaIntronic rs10861688 was associated with the number of depressive events corrected for the times patients were assessed during the period of observation. In particular, AA subjects (n=21) had 4.46±3.15 events, AG (n=141) had 3.08±3.17 and GG (n=342) 2.65±2.97 (p=0.0048, beta=-0.22). No other significant associations were reported. ConclusionaaWe bring further evidence that genes involved in the regulation of circadian rhythms may be relevant to depressive bipolar phases. Independent confirmation analyses are mandatory.
2
Investigation of an epistastic effect between a set of TAAR6 and HSP‐70 genes variations and major mood disorders

Pae, Chi‐,Un,Drago, Antonio,Forlani, Martina,Patkar, Ashwin A.,Serretti, Alessandro Wiley Subscription Services, Inc., A Wiley Company 2010 American Journal of Medical Genetics Part B: Neuro Vol. No.
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AbstractEpistasis, the interaction between genes, is a topic of current interest in molecular and quantitative genetics. We have further studied a previously investigated sample of 187 major depressive disorder (MDD) patients, 171 bipolar disorder (BD) patients, and 288 controls, and tried to analyze the interaction between a set of variations of independent genes: the trace amine receptor 6 (rs4305745, rs8192625, rs7452939, rs6903874, and rs6937506) and the heat shock protein 70 (rs562047, rs1061581, rs2227956). The multifactor dimensionality reduction (MDR) method was applied and the covariates associated with diagnosis were also controlled. A significant predictive value of specific interactions between genotypes located in the investigated genes was found. We then report preliminary evidence that the epistasis between trace amine receptor 6 and heat shock protein 70 variations may compose a risk profile for major mood disorders. The level of statistical significance (P < 0.001) and the testing balancing accuracy over 0.62 suggest a cautious optimism toward this result, although the possibility of false positivity warrants further analyses in independent samples. © 2009 Wiley‐Liss, Inc.
3
Effect of the Dysbindin Gene on Antimanic Agents in Patients with Bipolar I Disorder

Dong-Hwan Yun,Chi-Un Pae,Antonio Drago,Laura Mandelli,Diana De Ronchi,Ashwin A. Patkar,In Ho Paik,Alessandro Serretti,Jung-Jin Kim 대한신경정신의학회 2008 PSYCHIATRY INVESTIGATION Vol.5 No.2
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  ScienceON
  
  KCI
  
  스콜라
Objective: We previously reported an association between dysbindin gene (DTNBP1) variants and bipolar I disorder (BID). This paper expands upon previous findings suggesting that DTNBP1 variants may play a role in the response to acute mood stabilizer treatment. Methods: A total of 45 BID patients were treated with antimanic agents (lithium, valproate, or carbamazepine) for an average of 36.52 (±19.87) days. After treatment, the patients were evaluated using the Clinical Global Impression (CGI) scale and the Young Mania Rating Scale (YMRS) and genotyped for their DTNBP1 variants (rs3213207 A/G, rs1011313 C/T, rs2005976 G/A, rs760761 C/T and rs2619522 A/C). Results: There was no association between the variants investigated and response to mood stabilizer treatment, even after considering possible stratification factors. Conclusion: Although the small number of subjects is an important limitation in our study, DTNBP1 does not seem to be involved in acute antimanic efficacy. Objective: We previously reported an association between dysbindin gene (DTNBP1) variants and bipolar I disorder (BID). This paper expands upon previous findings suggesting that DTNBP1 variants may play a role in the response to acute mood stabilizer treatment. Methods: A total of 45 BID patients were treated with antimanic agents (lithium, valproate, or carbamazepine) for an average of 36.52 (±19.87) days. After treatment, the patients were evaluated using the Clinical Global Impression (CGI) scale and the Young Mania Rating Scale (YMRS) and genotyped for their DTNBP1 variants (rs3213207 A/G, rs1011313 C/T, rs2005976 G/A, rs760761 C/T and rs2619522 A/C). Results: There was no association between the variants investigated and response to mood stabilizer treatment, even after considering possible stratification factors. Conclusion: Although the small number of subjects is an important limitation in our study, DTNBP1 does not seem to be involved in acute antimanic efficacy.