title: Interaction effect of functional variants of the BDNF and DRD2/ANKK1 gene is associated with alexithymia in healthy human subjects.
abstract: OBJECTIVE
  To test the hypothesis that the interaction between the brain-derived neurotrophic factor (BDNF) and dopamine receptor D(2) (DRD2)/ANKK1 gene contributes to individual differences in alexithymia. The personality construct of alexithymia refers to difficulties in emotional self-regulation and contributes as a risk factor to several mental disorders. Alexithymic individuals show an impoverished conscious experience of emotions but an intact autonomic emotional response. Persons with high alexithymia scores reportedly show a reduced activation of the anterior cingulate cortex (ACC) during the processing of emotional stimuli. An interaction between two polymorphisms on the BDNF and DRD2/ANKK1 gene has been recently associated with reduced gray matter volume in the ACC and higher trait anxiety.
  
  
  METHODS
  We conducted a genetic association study. A total of 664 healthy participants completed the Toronto Alexithymia Scale questionnaire and were genotyped for the BDNF Val66Met (rs6265) and the DRD2/ANKK1 Taq IA (rs1800497) polymorphisms.
  
  
  RESULTS
  Carriers of at least one BDNF 66Met and one DRD2/ANKK1 A1 allele showed the highest scores in the total Toronto Alexithymia Scale and in the subscale "Difficulties Identifying Feelings."
  
  
  CONCLUSIONS
  In line with recent studies investigating the role of BDNF Val66Met and DRD2/ANKK1 Taq IA polymorphisms on anxiety and gray matter volume in the ACC, our findings provide the first evidence for a genetic contribution to alexithymia.
authors.affiliation: Department of Psychology, University of Bonn, Kaiser-Karl-Ring 9, Bonn, Germany. nora.walter@uni-bonn-diff.de
authors.forename: Nora T
authors.initials: NT
authors.lastname: Walter
authors.forename: Christian
authors.initials: C
authors.lastname: Montag
authors.forename: Sebastian A
authors.initials: SA
authors.lastname: Markett
authors.forename: Martin
authors.initials: M
authors.lastname: Reuter
mesh_terms: D000328:Adult; D000342:Affective Symptoms / Q000175:diagnosis / Q000235:genetics*; D017089:Ankyrin Repeat / Q000235:genetics*; D019208:Brain-Derived Neurotrophic Factor / Q000235:genetics*; D004644:Emotions / Q000502:physiology; D005260:Female; D056726:Genetic Association Studies; D014644:Genetic Variation; D005838:Genotype; D006179:Gyrus Cinguli / Q000033:anatomy & histology / Q000502:physiology; D006579:Heterozygote; D006801:Humans; D008297:Male; D008715:Methionine / Q000235:genetics; D010551:Personality / Q000235:genetics; D010555:Personality Inventory; D011110:Polymorphism, Genetic; D017346:Protein Serine-Threonine Kinases / Q000235:genetics*; D017448:Receptors, Dopamine D2 / Q000235:genetics*; D011795:Surveys and Questionnaires; D014633:Valine / Q000235:genetics
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D017448:Receptors, Dopamine D2; D008715:Methionine; C489948:ANKK1 protein, human; D017346:Protein Serine-Threonine Kinases; D014633:Valine