engleski

Genetyc study of monoamine oxidase type B in combat related posttraumatic stress disorder.

Introduction: Several neurobiological systems are dysfunctional in posttraumatic stress disorder (PTSD). An enzyme monoamine oxidase (MAO) occurs in two forms that differ in location, substrate and inhibitor specificities. MAO oxidizes different amines and neurotransmitters and regulates their concentration. Altered platelet MAO-B levels have been found in different psychopathologies, suggesting that it may be a biomarker for the particular disorders, personality traits and behaviors. The most common polymorphism of MAO-B gene is an A to G change, present in intron 13. The hypothesis was that PTSD would be associated with altered platelet MAO-B activity, due to the different distribution of the allele frequencies of the MAO-B genotype. Methods: Platelet MAO-B activity and MAO-B intron 13 polymorphism (a G/A substitution) were determined in 103 war veterans with DSM-IV diagnosed current and chronic PTSD, 41 combat exposed war veterans who did not develop PTSD, and 242 healthy control male subjects. PTSD patients were subdivided, according to the presence of psychotic symptoms (hallucinations or delusions on the psychotic module of the SCID, or specific disturbance in form of thoughts by mental status examination), assessed by the Positive and Negative Syndrome Scale, into subgroups of 28 patients with and 78 without psychotic features. Results: One-way ANOVAs showed that veterans with psychotic PTSD had significantly higher platelet MAO-B activity than veterans with or without PTSD, or healthy subjects, and that smokers had significantly lower platelet MAO-B activity than non-smokers in all groups. Two-way ANOVAs revealed significant effects of smoking, or diagnosis and smoking, but no significant effect of genotype, or interaction between genotype, smoking or diagnosis, on platelet MAO-B activity. The allele frequencies of the MAO-B genotype were similarly distributed among healthy controls and veterans with or without PTSD and/or psychotic symptoms. Conclusion: The MAO-B intron 13 polymorphism was not functional, and did not affect platelet MAO-B activity, indicating that other polymorphisms should be assessed to determine functional significance and associations with different traits or disease. The results suggest that platelet MAO-B activity, controlled for smoking status, might be used as a peripheral marker of the psychotic symptoms in PTSD.

MAO-B intron 13 polymorphism; platelet MAO-B activity; PTSD

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