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Updated: May 15, 2026

Exploring the Neural Correlates of Cognitive Reappraisal in Obsessive-Compulsive Disorder Using Task-based Functional Magnetic Resonance Imaging
Published on: March 14, 2025
Common genetic background in anorexia nervosa and obsessive compulsive disorder: preliminary results from an
Sergi Mas1, Maria Teresa Plana, Josefina Castro-Fornieles
1Department of Anatomic Pathology, Pharmacology and Microbiology, University of Barcelona, Spain. sergimash@ub.edu
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 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.
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