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Bersani F.S.,University of California at San Francisco | Bersani F.S.,University of Rome La Sapienza | Morley C.,University of California at San Francisco | Lindqvist D.,University of California at San Francisco | And 15 more authors.
Progress in Neuro-Psychopharmacology and Biological Psychiatry | Year: 2016

Introduction: Mitochondrial abnormalities may be involved in PTSD, although few studies have examined this. Mitochondrial DNA copy number (mtDNAcn) in blood cells is an emerging systemic index of mitochondrial biogenesis and function. The present study assessed mtDNAcn in male combat-exposed veterans with PTSD compared to those without PTSD as well as its correlation with clinical scales. Methods: mtDNAcn was assessed with a TaqMan multiplex assay in granulocytes of 43 male combat veterans with (n. =43) or without (n. =44) PTSD. Twenty of the PTSD subjects had co-morbid major depressive disorder (MDD). The Clinician Administered PTSD Scale (CAPS), the Positive and Negative Affect Schedule (PANAS), the Early Trauma Inventory (ETI) and the Beck Depression Inventory II (BDI-II) were used for the clinical assessments. All analyses were corrected for age and BMI. Results: mtDNAcn was significantly lower in subjects with PTSD (p. <. 0.05). Within the PTSD group, those with moderate PTSD symptom severity had relatively higher mtDNAcn than those with mild or severe symptoms (p. <. 0.01). Within the PTSD group, mtDNAcn was positively correlated with PANAS positive subscale ratings (p. <. 0.01) but was not significantly correlated with PANAS negative subscale, ETI or BDI-II ratings. Discussion: This study provides the first evidence of: (i) a significant decrease of mtDNAcn in combat PTSD, (ii) a possible "inverted-U" shaped relationship between PTSD symptom severity and mtDNAcn within PTSD subjects, and (iii) a direct correlation of mtDNAcn with positive affectivity within PTSD subjects. Altered mtDNAcn in PTSD may reflect impaired energy metabolism, which might represent a novel aspect of its pathophysiology. © 2015 Elsevier Inc. Source

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