BDNF and COMT polymorphisms have a limited association with episodic memory performance or engagement in complex cognitive activity in healthy older adults.
Cognitive decline is a major factor in lowering the quality of life in older populations, and contributes substantially to social, economic, and health costs. As humans age, cognitive function decreases differentially, and individual differences in cognitive ageing are likely attributed to a range of causes, including environmental and genetic influences. The current study included 360 participants (240 females and 120 males) aged between 50 and 79years from the Tasmanian Healthy Brain Project. The brain-derived neurotrophic factor (BDNF) Val66Met and Catechol-O-Methyltransferase (COMT) Val158Met polymorphisms were examined for their association with visual and auditory episodic memory performance. The polymorphisms were also investigated for their association with reported life-long engagement in complex cognitive activity using a retrospective questionnaire. Relative to the demographic variables, the gene variations were found to have no association with episodic memory performance, with the exception of the COMT polymorphism on a single measure of auditory memory (RAVLT). Several other studies also demonstrated that these polymorphisms have no, small, or inconsistent effects on memory function. The BDNF Val66Met and COMT Val158Met polymorphisms were also found to be of little significance to active engagement in complex cognitive activity throughout most of the lifespan. An association was detected between BDNF Val66Met and engagement in cognitive activity in early life (p=.04, d=.23), however this did not reach significance when adjusted for multiple comparisons. The biological mechanisms that underlie engagement in cognitive activity are elusive, thus the potential relationship between BDNF Val66Met genotype and early life cognitive engagement warrants further investigation.
Wicking Dementia Research and Education Centre, University of Tasmania, Australia; School of Medicine, University of Tasmania, Tasmania, Australia.
Kimberley
K
Stuart
Wicking Dementia Research and Education Centre, University of Tasmania, Australia; School of Psychology, University of Tasmania, Tasmania, Australia. Electronic address: Mathew.Summers@utas.edu.au.
Mathew James
MJ
Summers
Regenerative Neuroscience Group, Brain and Mind Research Institute, University of Sydney, Australia.
Michael J
MJ
Valenzuela
Wicking Dementia Research and Education Centre, University of Tasmania, Australia; School of Medicine, University of Tasmania, Tasmania, Australia.
James C
JC
Vickers
D000368:Aged; D000375:Aging / Q000523:psychology; D019208:Brain-Derived Neurotrophic Factor / Q000235:genetics*; D002394:Catechol O-Methyltransferase / Q000235:genetics*; D003071:Cognition / Q000502:physiology*; D005260:Female; D056726:Genetic Association Studies; D005838:Genotype; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D061212:Memory, Episodic; D008875:Middle Aged; D009483:Neuropsychological Tests; D011446:Prospective Studies
D019208:Brain-Derived Neurotrophic Factor; C588010:COMT protein, human; D002394:Catechol O-Methyltransferase
Ageing; BDNF; COMT; Cognition; LEQ; Memory