Ana M Peiró1, María S García-Gutiérrez2,3, Beatriz Planelles4, Teresa Femenía2, Carlos Mingote5, Luis Jiménez-Treviño6, Sara Martínez-Barrondo6, M Paz García-Portilla6, Pilar A Saiz6, Julio Bobes6, Jorge Manzanares2,3. 1. Clinical Pharmacology Unit and Neuropharmacology on Pain and Functional Diversity (NED), Department of Health of Alicante - General Hospital, ISABIAL, Alicante, Spain. 2. Neuroscience Institute, Alicante, Miguel Hernández University, San Juan de Alicante, Spain. 3. Cooperative Networking in Health Research (RETICS-addictive disorders), Health Institute Carlos III, MICINN and FEDER, Madrid, Spain. 4. Research Unit, Hospital General Hospital, Alicante, Spain. 5. University Hospital 12 de Octubre, Madrid, Spain. 6. Psychiatry Department, Medicine Faculty, University of Oviedo; Biomedical Research Centre in Mental Health Network (CIBERSAM); University Institute of Neuroscience of Asturias, INEUROPA; Health Service of Asturias, SESPA, Asturias, Spain.
Abstract
Background and objectives: Panic disorder (PD) is an anxiety disorder characterized by recurrent and unexpected panic attacks along with sudden onset of apprehension, fear or terror. The endocannabinoid system (ECS) has a role in stress recovery, regulating anxiety. The aim of this study was to analyze potential genetic alterations in key ECS targets in patients suffering from panic disorders.Design and methods: We analyzed single nucleotide polymorphisms (SNPs) of the cannabinoid receptors (CNR1; CNR2) and the endocannabinoid hydrolytic enzyme fatty acid amide hydrolase (FAAH) genes in 164 Spanish PD patients and 320 matched controls. Results: No significant differences were observed in the SNPs of the CNR2 and FAAH genes tested. However, when analyzing genotype-by-sex interaction at A592G (rs2501431) and C315T (rs2501432) in the CNR2 gene, the presence of the G-allele in males was associated with a protective haplotype. Genotyping analysis revealed that variants in CNR1 confer vulnerability to PD, with a significantly increased risk associated with the G-allele (rs12720071) and C-allele (rs806368). This finding was consistent when analyzing genotype-by-sex interaction, where females presented a greater PD risk.Conclusions: Polymorphisms at the CNR1 gene may be a risk factor for PD contributing to sex-specific dysfunction in females.
Background and objectives: Panic disorder (PD) is an anxiety disorder characterized by recurrent and unexpected panic attacks along with sudden onset of apprehension, fear or terror. The endocannabinoid system (ECS) has a role in stress recovery, regulating anxiety. The aim of this study was to analyze potential genetic alterations in key ECS targets in patients suffering from panic disorders.Design and methods: We analyzed single nucleotide polymorphisms (SNPs) of the cannabinoid receptors (CNR1; CNR2) and the endocannabinoid hydrolytic enzyme fatty acid amide hydrolase (FAAH) genes in 164 Spanish PDpatients and 320 matched controls. Results: No significant differences were observed in the SNPs of the CNR2 and FAAH genes tested. However, when analyzing genotype-by-sex interaction at A592G (rs2501431) and C315T (rs2501432) in the CNR2 gene, the presence of the G-allele in males was associated with a protective haplotype. Genotyping analysis revealed that variants in CNR1 confer vulnerability to PD, with a significantly increased risk associated with the G-allele (rs12720071) and C-allele (rs806368). This finding was consistent when analyzing genotype-by-sex interaction, where females presented a greater PD risk.Conclusions: Polymorphisms at the CNR1 gene may be a risk factor for PD contributing to sex-specific dysfunction in females.