title: Polymorphisms of BDNF and CACNA1C are not associated with cognitive functioning in bipolar disorder or healthy controls.
abstract: The cause of cognitive dysfunction in bipolar disorder (BD) is not well understood. BDNF and CACNA1C are two susceptibility genes for the disorder that have also been reported to be associated with cognitive deficits in the disorder, but the studies have been small and with conflicting results. We therefore attempted to replicate an association between cognitive dysfunction with the most commonly studied single nucleotide polymorphisms rs6265 and rs1006737.
  
  
  
  Regression models with five aggregated cognitive domains derived from a comprehensive test battery and IQ score were run using directly genotyped risk variants of SNPs rs6265 and rs1006737 as predictors with covariates as appropriate. Models were performed in a clinical sample of Swedish patients with BD (N = 114) and sex- and age-matched population controls (N = 104).
  
  
  
  No significant associations (regardless of correction for multiple testing) between the BDNF and CACNA1C risk variants and cognitive functioning were found in either patients or controls.
  
  
  
  Our results do not support that the common genetic risk variants in rs6265 and rs1006737 are associated with cognitive dysfunction.
authors.affiliation: a Institute of Neuroscience and Physiology , The Sahlgrenska Academy at the Gothenburg University , Gothenburg , Sweden.
authors.forename: Sindre
authors.initials: S
authors.lastname: Rolstad
authors.affiliation: b Department of Medical Epidemiology and Biostatistics , Karolinska Institutet , Stockholm , Sweden.
authors.forename: Carl
authors.initials: C
authors.lastname: Sellgren Majkowitz
authors.affiliation: a Institute of Neuroscience and Physiology , The Sahlgrenska Academy at the Gothenburg University , Gothenburg , Sweden.
authors.forename: Erik
authors.initials: E
authors.lastname: Joas
authors.affiliation: c Department of Clinical Neuroscience , Karolinska Institutet , Stockholm , Sweden.
authors.forename: Carl Johan
authors.initials: CJ
authors.lastname: Ekman
authors.affiliation: a Institute of Neuroscience and Physiology , The Sahlgrenska Academy at the Gothenburg University , Gothenburg , Sweden.
authors.forename: Erik
authors.initials: E
authors.lastname: Pålsson
authors.affiliation: a Institute of Neuroscience and Physiology , The Sahlgrenska Academy at the Gothenburg University , Gothenburg , Sweden.|b Department of Medical Epidemiology and Biostatistics , Karolinska Institutet , Stockholm , Sweden.|c Department of Clinical Neuroscience , Karolinska Institutet , Stockholm , Sweden.
authors.forename: Mikael
authors.initials: M
authors.lastname: Landén
mesh_terms: D000328:Adult; D001714:Bipolar Disorder / Q000235:genetics / Q000503:physiopathology*; D019208:Brain-Derived Neurotrophic Factor / Q000235:genetics*; D020746:Calcium Channels, L-Type / Q000235:genetics*; D016022:Case-Control Studies; D003072:Cognition Disorders / Q000235:genetics / Q000503:physiopathology*; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D020641:Polymorphism, Single Nucleotide; D013548:Sweden; D044465:White People / Q000235:genetics
chemical_list: D019208:Brain-Derived Neurotrophic Factor; C079146:CACNA1C protein, human; D020746:Calcium Channels, L-Type
keywords: Single nucleotide polymorphisms; bipolar disorder; cognition