COMT, BDNF, and DTNBP1 polymorphisms and cognitive functions in patients with brain tumors Academic Article uri icon


MeSH Major

  • Brain Neoplasms
  • Brain-Derived Neurotrophic Factor
  • Catechol O-Methyltransferase
  • Cognition Disorders
  • Dystrophin-Associated Proteins


  • © 2016 The Author(s) 2016. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved.Background Cognitive dysfunction is common among patients with brain tumors and can be associated with the disease and treatment with radiotherapy and chemotherapy. However, little is known about genetic risk factors that may moderate the vulnerability for developing cognitive dysfunction. In this study, we examined the association of single nucleotide polymorphisms (SNPs) in the catechol-O-methyl transferase (COMT), brain-derived neurotrophic factor (BDNF), and dystrobrevin-binding protein 1 (DTNBP1) genes with cognitive functions and neuroimaging outcomes in patients with brain tumors. Methods One hundred and fifty patients with brain tumors completed neuropsychological tests of attention, executive functions, and memory and were genotyped for polymorphisms in the COMT, BDNF, and DTNBP1 genes. Ratings of white matter (WM) abnormalities on magnetic resonance imaging scans were performed. Results Multivariate regression shrinkage analyses, adjusted for age, education, treatment type, time since treatment completion, and tumor location, indicated a significant association between the COMT SNP rs4680 (Val158Met) and memory with lower scores in delayed recall (P <. 01) among homozygotes (valine/valine). Additional COMT, BDNF and DTNBP1 SNPs were significantly associated with attention, executive functions, and memory scores. Conclusion This is the first study to suggest that known and newly described polymorphisms in genes associated with executive and memory functions in healthy individuals and other clinical populations may modulate cognitive outcome in patients with brain tumors.

publication date

  • October 2016



  • Academic Article



  • eng

PubMed Central ID

  • PMC5035520

Digital Object Identifier (DOI)

  • 10.1093/neuonc/now057

PubMed ID

  • 27091610

Additional Document Info

start page

  • 1425

end page

  • 1433


  • 18


  • 10