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

• Published in: Journal of psychiatric research 2013-06, Vol.47 (6), p.747-754
• Main Authors: Mas, Sergi, Plana, Maria Teresa, Castro-Fornieles, Josefina, Gassó, Patricia, Lafuente, Amalia, Moreno, Elena, Martinez, Esteban, Milà, Montserrat, Lazaro, Luisa
• Format: Article
• Language: English
• Subjects: Adolescent; Adult and adolescent clinical studies; Anorexia nervosa; Anorexia Nervosa - genetics; Anxiety disorders. Neuroses; Biological and medical sciences; Candidate genes; Candidates; Child; Cohort Studies; Eating behavior disorders; Female; Genes; Genetic Association Studies - methods; Genetic association study; Genetic Markers - physiology; Genetic Predisposition to Disease - genetics; Glutamate; Glutamic Acid - genetics; Humans; Male; Medical sciences; Neurodevelopment; Obsessive compulsive disorder; Obsessive-Compulsive Disorder - genetics; Obsessive-compulsive disorders; Obsessive-Compulsive neuroses; Pilot Projects; Polymorphism, Single Nucleotide - genetics; Psychiatry; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Serotonin; Serotonin - genetics; Variants
• ISSN: 0022-3956; 1879-1379
• DOI: 10.1016/j.jpsychires.2012.12.015

Abstract 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 × 10−3 , rs4825476 ( GRIA3 ) p  = 4 × 10−4 , and rs1074815 ( TPH2 ) p  = 8 × 10−4 ) and 2 additional polymorphisms showing nominal significance (rs2834070 ( OLIG2 ) p  = 2 × 10−3 and rs11783752 ( SCL18A1 ) p  = 3 × 10−3 ), were found to be related to both AN and OCD. In addition, rs3825885 ( NTRK3 , p  = 9 × 10−4 ) was identified as an AN risk variant, and rs11179027 ( TPH2 , p  = 2 × 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 SLC18A 1) 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.