Tamsyn E Van Rheenen1, Susan L Rossell. 1. Brain and Psychological Sciences Research Centre, Faculty of Life and Social Sciences, Swinburne University, and Cognitive Neuropsychology Laboratory, Monash Alfred Psychiatry Research Center, The Alfred Hospital, Melbourne, Australia. tvanrheenen@swin.edu.au
Abstract
INTRODUCTION: Bipolar Disorder (BD) is a serious mood disorder, the aetiology of which is still unclear. The disorder is characterised by extreme mood variability in which patients fluctuate between markedly euphoric, irritable, and elevated states to periods of severe depression. The current research literature shows that BD patients demonstrate compromised neurocognitive ability in addition to these mood symptoms. Viable candidate genes implicated in neurocognitive and socioemotional processes may explain the development of these core emotion abnormalities. Additionally, links between faulty neurocognition and impaired socioemotional ability complement genetic explanations of BD pathogenesis. This review examines associations between cognition indexing prefrontal neural regions and socioemotional impairments including emotion processing and regulation. A review of the effect of COMT and TPH2 on these functions is also explored. METHODS: Major computer databases including PsycINFO, Google Scholar, and Medline were consulted in order to conduct a comprehensive review of the genetic and cognitive literature in BD. RESULTS: This review determines that COMT and TPH2 genetic variants contribute susceptibility to abnormal prefrontal neurocognitive function which oversees the processing and regulation of emotion. This provides for greater understanding of some of the emotional and cognitive symptoms in BD. CONCLUSIONS: Current findings in this direction show promise, although the literature is still in its infancy and further empirical research is required to investigate these links explicitly.
INTRODUCTION:Bipolar Disorder (BD) is a serious mood disorder, the aetiology of which is still unclear. The disorder is characterised by extreme mood variability in which patients fluctuate between markedly euphoric, irritable, and elevated states to periods of severe depression. The current research literature shows that BD patients demonstrate compromised neurocognitive ability in addition to these mood symptoms. Viable candidate genes implicated in neurocognitive and socioemotional processes may explain the development of these core emotion abnormalities. Additionally, links between faulty neurocognition and impaired socioemotional ability complement genetic explanations of BD pathogenesis. This review examines associations between cognition indexing prefrontal neural regions and socioemotional impairments including emotion processing and regulation. A review of the effect of COMT and TPH2 on these functions is also explored. METHODS: Major computer databases including PsycINFO, Google Scholar, and Medline were consulted in order to conduct a comprehensive review of the genetic and cognitive literature in BD. RESULTS: This review determines that COMT and TPH2 genetic variants contribute susceptibility to abnormal prefrontal neurocognitive function which oversees the processing and regulation of emotion. This provides for greater understanding of some of the emotional and cognitive symptoms in BD. CONCLUSIONS: Current findings in this direction show promise, although the literature is still in its infancy and further empirical research is required to investigate these links explicitly.