BACKGROUND: The neurobiology of posttraumatic stress disorder (PTSD) involves alterations in multiple neuroendocrine and neurotransmitter systems. Platelet monoamine oxidase (MAO-B) has been associated with susceptibility to various psychiatric disorders, personality traits and behaviors. METHODS: Platelet MAO-B activity and MAO-B intron 13 polymorphism (a G/A substitution) were determined in male war veterans (n=106) with DSM-IV diagnosed current and chronic PTSD, divided into subgroups of PTSD patients with (n=28) or without (n=78) psychotic features, combat exposed veterans (n=41) who did not develop PTSD, and healthy control men (n=242). RESULTS: Two-way ANOVAs revealed a significant effect of diagnosis and smoking, a significant effect of smoking, no significant effect of genotype, and no significant interaction between genotype, smoking or diagnosis, on platelet MAO-B activity. One-way ANOVAs showed significantly lower platelet MAO-B activity in smokers than in nonsmokers. After controlling for smoking, veterans with psychotic PTSD had significantly higher platelet MAO-B activity than veterans with or without PTSD, or healthy subjects. LIMITATIONS: The results were obtained on peripheral biochemical marker, i.e. platelet MAO activity. CONCLUSIONS: The MAO-B intron 13 polymorphism was not functional, and did not affect 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. 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.
BACKGROUND: The neurobiology of posttraumatic stress disorder (PTSD) involves alterations in multiple neuroendocrine and neurotransmitter systems. Platelet monoamine oxidase (MAO-B) has been associated with susceptibility to various psychiatric disorders, personality traits and behaviors. METHODS: Platelet MAO-B activity and MAO-B intron 13 polymorphism (a G/A substitution) were determined in male war veterans (n=106) with DSM-IV diagnosed current and chronic PTSD, divided into subgroups of PTSDpatients with (n=28) or without (n=78) psychotic features, combat exposed veterans (n=41) who did not develop PTSD, and healthy control men (n=242). RESULTS: Two-way ANOVAs revealed a significant effect of diagnosis and smoking, a significant effect of smoking, no significant effect of genotype, and no significant interaction between genotype, smoking or diagnosis, on platelet MAO-B activity. One-way ANOVAs showed significantly lower platelet MAO-B activity in smokers than in nonsmokers. After controlling for smoking, veterans with psychotic PTSD had significantly higher platelet MAO-B activity than veterans with or without PTSD, or healthy subjects. LIMITATIONS: The results were obtained on peripheral biochemical marker, i.e. platelet MAO activity. CONCLUSIONS: The MAO-B intron 13 polymorphism was not functional, and did not affect 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. 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.
Authors: Abdalla Bowirrat; Thomas J H Chen; Kenneth Blum; Margaret Madigan; John A Bailey; Amanda Lih Chuan Chen; B William Downs; Eric R Braverman; Shahien Radi; Roger L Waite; Mallory Kerner; John Giordano; Siohban Morse; Marlene Oscar-Berman; Mark Gold Journal: Curr Neuropharmacol Date: 2010-12 Impact factor: 7.363
Authors: Sabah Nisar; Ajaz A Bhat; Sheema Hashem; Najeeb Syed; Santosh K Yadav; Shahab Uddin; Khalid Fakhro; Puneet Bagga; Paul Thompson; Ravinder Reddy; Michael P Frenneaux; Mohammad Haris Journal: Int J Mol Sci Date: 2020-06-24 Impact factor: 5.923