LAUSR

To the Editor, Obstructive sleep apnea (OSA) is caused by repetitive intermittent hypoxia and re-oxygenation during sleep and has been associated with an increased risk of many adverse health outcomes, including cognitive impairment, cardiovascular events, stroke, and depression. OSA is effectively treated by continuous positive airway pressure (CPAP) therapy [1], which protects pharyngeal airway to improve oxygenation during sleep. CPAP therapy can normalize sleep parameters of OSA and also ameliorate depressive symptoms. However, mechanisms underlying the effect of CPAP therapy on improvements of sleep parameters and/or depressive symptoms remain to be unclear. Brain-derived neurotrophic factor (BDNF), one of neurotrophins, has various important roles in the brain. In addition to its neurotrophic actions, mature BDNF plays important roles in the regulation of glucose and lipid metabolism or the energy homeostasis in peripheral organs [2]. Accumulating evidence shows that serum BDNF levels are decreased in psychiatric and metabolic disorders, including sleep disorders, depression, obesity, type 2 diabetes mellitus, and cardiovascular diseases [2, 3]. Moreover, proBDNF is converted to mature BDNF by proteases, such as matrix metalloproteinases and/or plasmin. Interaction of mature BDNF with TrkB receptors promotes cell survival, while binding of proBDNF to p75 neurotrophin receptor induces apoptosis, suggesting that proBDNF and mature BDNF induce complete opposite biological responses [3]. Thus, further works to measure both mature BDNF and proBDNF will be needed to elucidate the functional roles of BDNF on psychiatric and metabolic disorders [3]. To our knowledge, only one study has measured the change of BDNF signaling during CPAP therapy in OSA patients [4]. This is the first report to focus on the relationships among sleep parameters, depressive symptoms, and BDNF signaling in OSA patients during CPAP therapy, suggesting that baseline mature BDNF levels might predict the amelioration of SpO2% after the CPAP therapy. The result was obtained from a prospective trial with consecutive enrollment of patients who were recruited from July 1, 2012, to June 30, 2014. We recruited patients who were suffered from OSA to take home sleep test using the LS-100 device. Subsequently, we had selected patients suffering from moderate/severe OSA, whose apnea–hypopnea index (AHI) > 15, using full-night polysomnography (PSG). We had treated patients who presented AHI > 20 by CPAP therapy for 3 months. We scored sleep stages and respiratory parameters in reference to the standard criteria of the American Academy of Sleep Medicine. Although we enrolled 95 patients with suspected OSA and 29 patients who received CPAP therapy for 3 months, we evaluated 19 patients who presented both Geriatric Depression Scale (GDS), a 15-item self-rating depression screening scale, and serum samples before and after CPAP therapy in this study. None of CPAP compliant patients was previously prescribed or using antidepressant drug therapy over the course of this study. This study was approved by the Institutional Review Board of Human Research at Saga University, and we obtained written informed consents from all participants. We measured serum levels of proBDNF and mature BDNF by the human proBDNF and BDNFELISAKits (Adipo Bioscience, Santa Clara, CA, USA). Measurements were performed according to the manufacturer’s instructions and based on our experiences as previously reported. We used the Statistical Package for the Social Sciences (SPSS) software for statistical analyses. Statistical significance was determined * Yoshito Mizoguchi [email protected]