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BDNF function as a potential mediator of bipolar disorder and post-traumatic stress disorder comorbidity

Abstract

Bipolar disorder (BD) and post-traumatic stress disorder (PTSD) frequently co-occur among psychiatric patients, leading to increased morbidity and mortality. Brain-derived neurotrophic factor (BDNF) function is associated with core characteristics of both BD and PTSD. We propose a neurobiological model that underscores the role of reduced BDNF function resulting from several contributing sources, including the met variant of the BDNF val66met (rs6265) single-nucleotide polymorphism, trauma-induced epigenetic regulation and current stress, as a contributor to the onset of both illnesses within the same person. Further studies are needed to evaluate the genetic association between the val66met allele and the BD-PTSD population, along with central/peripheral BDNF levels and epigenetic patterns of BDNF gene regulation within these patients.

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Acknowledgements

Dr Dunlop is supported by a K23 award (K23MH086690). Over the past 3 years, Dr Rakofsky has received research support from AstraZeneca and Novartis. Dr Ressler is a co-founder of Extinction Pharmaceuticals, LLC, but has received no financial or research support within the past 3 years from this arrangement. Dr Dunlop has received research support from AstraZeneca, Evotec, Forest, Glaxo-Smith-Kline, Ono Pharmaceuticals, Pfizer, Takeda and Wyeth. He has also served as a consultant to Imedex and MedAvante.

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Rakofsky, J., Ressler, K. & Dunlop, B. BDNF function as a potential mediator of bipolar disorder and post-traumatic stress disorder comorbidity. Mol Psychiatry 17, 22–35 (2012). https://doi.org/10.1038/mp.2011.121

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