4.6 Article

Common genetic background in anorexia nervosa and obsessive compulsive disorder: Preliminary results from an association study

期刊

JOURNAL OF PSYCHIATRIC RESEARCH
卷 47, 期 6, 页码 747-754

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jpsychires.2012.12.015

关键词

Anorexia nervosa; Obsessive compulsive disorder; Genetic association study; Candidate genes; Glutamate; Serotonin; Neurodevelopment

资金

  1. Carlos III Research Institute of the Spanish Ministry of Health [FIS PI070350]
  2. Sara Sorrell contract [CD09/00296]
  3. Generalitat de Catalunya [2009 SGR 1119, 2009 SGR 1295, 2009 SGR 1501]

向作者/读者索取更多资源

Several lines of evidence, including psychopathological, neurobiological, pharmacological and epidemiological data, supported the association between Anorexia Nervosa (AN) and Obsessive-Compulsive Disorder (OCD). The aim of the present study is to test the hypothesis of partial common genetic background of both disease, AN and OCD. A total of 116 patients with AN, 74 patients with OCD and 91 controls participated in this study. 213 single-nucleotide polymorphisms (SNPs) in 28 candidate genes were analyzed. Five SNPs achieved 0.004 (the nominal p-value expected by chance), 3 with empirical significant p-values (rs10070190 (CDH9) p = 1 x 10(-3), rs4825476 (GRIA3)p = 4 x 10(-4), and rs1074815 (TPH2) p = 8 x 10(-4)) and 2 additional polymorphisms showing nominal significance (rs2834070 (OLIG2) p = 2 x 10(-3) and rs11783752 (SCL18A1) p = 3 x 10-3), were found to be related to both AN and OCD. In addition, rs3825885 (NTRK3, p = 9 x 10-4) was identified as an AN risk variant, and rs11179027 (TPH2, p = 2 x 10-3) as an OCD marker. The ROC analysis confirmed these results and showed interaction among the significant SNPs. The preliminary results we report here reveal a partial common genetic background in AN and OCD, in agreement with previous clinical findings of common symptomathology between these two diseases and open the field of possible treatments for AN. The interaction observed between the associated polymorphisms, could indicate that there is a biological interaction between the serotonin (TPH2 and SLC18A1) and glutamate (GRIA3) pathways and the factors related to neurogenesis (CDH9, OLIG2 and NTRK3) for the explanation of etiopathophysiology in both diseases. However, the results must be replicated in studies with larger cohorts in order to confirm these associations. (C) 2013 Elsevier Ltd. All rights reserved.

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