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

Journal

MOLECULAR PSYCHIATRY
Volume 17, Issue 1, Pages 22-35

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/mp.2011.121

Keywords

bipolar disorder; post-traumatic stress disorder; brain-derived neurotrophic factor

Funding

  1. K23 award [K23MH086690]
  2. AstraZeneca
  3. Novartis
  4. Evotec
  5. Forest
  6. GlaxoSmith-Kline
  7. Ono Pharmaceuticals
  8. Pfizer
  9. Takeda
  10. Wyeth
  11. NATIONAL CENTER FOR ADVANCING TRANSLATIONAL SCIENCES [UL1TR000454] Funding Source: NIH RePORTER
  12. NATIONAL CENTER FOR RESEARCH RESOURCES [UL1RR025008] Funding Source: NIH RePORTER
  13. NATIONAL INSTITUTE OF MENTAL HEALTH [K23MH086690] Funding Source: NIH RePORTER

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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. Molecular Psychiatry (2012) 17, 22-35; doi:10.1038/mp.2011.121; published online 20 September 2011

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