there have been reported reduced mitochondrial respiration, maximal capacity of the electron transport, and respiratory rate after a complex I inhibition. A decrement in mitochondrial respiration and capacity of
the electron transport system in platelet was involved in the decrease in the availability of oxidative phosphorylation (OXPHOS) substrates and coenzymes in partially remitted patients [10]. BMCs had significantly lower basal and maximal respiratory rates than controls [10]. Our preliminary data suggest that reduced mitochondrial biogenesis could account for the lower respiratory, bio-energetic levels, and mtDNA deletion in MDD. Furthermore, because oxidative stress is likely involved in the pathophysiology of MDD, it has been shown that PGC-1a induction by phosphorylation of AMPK increases MnSOD and catalase expression levels [1]. Consistent with this model, our study proposes the mitochondrial biogenesis induction as the basis for a valuable new therapeutic target/strategy. Future research should
be focused on studying the significance of mitochondrial biogenesis in MDD etiology and as a potential therapeutic target. In this sense, mitochondrial biogenesis activators, such as CoQ10, metformin,
AICAR, resveratrol, caloric restriction, or physical activity, can provide new therapeutic opportunities.
Acknowledgments This work has been supported by Grupo de Investigacion Junta de Andalucia CTS113, Conseje_na de Salud of the Junta de Andalucia (PI-0036-2014). MRC-UK PET Methodology Programme Grant G1100809/1.
Competing Interests
The authors declared that they have no competing interests.