title: Inflammatory mediators of cognitive impairment in bipolar disorder.
abstract: OBJECTIVE
  Recent studies have pointed to neuroinflammation, oxidative stress and neurotrophic factors as key mediators in the pathophysiology of mood disorders. Little is however known about the cascade of biological episodes underlying the cognitive deficits observed during the acute and euthymic phases of bipolar disorder (BD). The aim of this review is to assess the potential association between cognitive impairment and biomarkers of inflammation, oxidative stress and neurotrophic activity in BD.
  
  
  METHODS
  Scopus (all databases), Pubmed and Ovid Medline were systematically searched with no language or year restrictions, up to November 2013, for human studies that collected both inflammatory markers and cognitive data in BD. Selected search terms were bipolar disorder, depression, mania, psychosis, inflammatory, cognitive and neurotrophic.
  
  
  RESULTS
  Ten human studies satisfied the criteria for consideration. The findings showed that high levels of peripheral inflammatory-cytokine, oxidative stress and reduced brain derived neurotrophic factor (BDNF) levels were associated with poor cognitive performance. The BDNF val66met polymorphism is a potential vulnerability factor for cognitive impairment in BD.
  
  
  CONCLUSIONS
  Current data provide preliminary evidence of a link between the cognitive decline observed in BD and mechanisms of neuroinflammation and neuroprotection. The identification of BD specific inflammatory markers and polymorphisms in inflammatory response genes may be of assistance for therapeutic intervention.
authors.affiliation: University of Texas Health Science Center at Houston, Department of Psychiatry and Behavioral Sciences, 77054 Houston, TX, United States. Electronic address: Isabelle.E.Bauer@uth.tmc.edu.
authors.forename: Isabelle E
authors.initials: IE
authors.lastname: Bauer
authors.affiliation: Department of Clinical Neuroscience and Rehabilitation, Sahlgrenska Academy at University of Gothenburg, Box 440, 40530 Gothenburg, Sweden.
authors.forename: Michaela C
authors.initials: MC
authors.lastname: Pascoe
authors.affiliation: Laboratório de Psiquiatria Molecular, Instituto Nacional de Ciência e Tecnologia - Translacional em Medicina (INCT), Hospital de Clínicas de Porto Alegre, Programa de Pós-Graduação em Ciências Biológicas: Bioquímica, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
authors.forename: Bianca
authors.initials: B
authors.lastname: Wollenhaupt-Aguiar
authors.affiliation: University of Texas Health Science Center at Houston, Department of Psychiatry and Behavioral Sciences, 77054 Houston, TX, United States; Laboratório de Psiquiatria Molecular, Instituto Nacional de Ciência e Tecnologia - Translacional em Medicina (INCT), Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
authors.forename: Flavio
authors.initials: F
authors.lastname: Kapczinski
authors.affiliation: University of Texas Health Science Center at Houston, Department of Psychiatry and Behavioral Sciences, 77054 Houston, TX, United States.
authors.forename: Jair C
authors.initials: JC
authors.lastname: Soares
mesh_terms: D001714:Bipolar Disorder / Q000150:complications* / Q000235:genetics / Q000276:immunology*; D003072:Cognition Disorders / Q000150:complications* / Q000235:genetics / Q000276:immunology*; D006801:Humans; D015213:Neuroimmunomodulation / Q000235:genetics / Q000502:physiology
keywords: Bipolar disorder; Cognitive functioning; Neuroinflammation; Neurotrophin; Oxidative stress