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Environmental and genetic contributors to cognitive reserve

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Ward, DD (2015) Environmental and genetic contributors to cognitive reserve. PhD thesis, University of Tasmania.

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Abstract

An individual’s rate of age-related cognitive decline and risk for later-life dementia is
influenced by environmental and genetic factors. One protective environmental factor that
may mitigate cognitive decline is cognitive reserve (CR) and is generated by participation in
tasks that involve complex cognitive engagement. Two genes that may influence CR through
their associations with synaptic plasticity are apolipoprotein E (APOE) and brain-derived
neurotrophic factor (BDNF). Participants from the on-going Tasmanian Healthy Brain
Project, a longitudinal investigation into whether an intervention of later-life tertiary
education increases CR, contributed to the data analysed in this thesis. It was aimed: to
develop two operational measures of CR; to quantify the cognitive implications of variation in
APOE and BDNF Val66Met; and to detect genetic interactions with CR. Comprehensive
neuropsychological assessments were conducted as part of the baseline testing for Tasmanian
Healthy Brain Project participants. APOE and BDNF Val66Met polymorphisms were
determined through analysis of saliva samples. The statistical analyses yielded three main
results. First, factor analysis was successful in identifying latent variables in both prior and
current models of CR. Second, while variation in APOE or BDNF did not produce significant
main effects in any assessed cognitive domain, an APOE x BDNF interaction was present in
episodic memory function. Third, BDNF moderated the association between CR and
executive function, with a significantly reduced association between the variables present in
BDNF Met carriers. Overall, this investigation developed a method of assessing CR that can
provide a comprehensive estimate of an individual’s CR and furthered knowledge on the
effect single genes exert on healthy cognitive function. The most important finding to emerge
was a CR x BDNF interaction in cognitive function, which suggests that CR-based
interventions aimed at delaying dementia onset may have a higher efficacy in BDNF Val
homozygotes than in BDNF Met carriers.

Item Type: Thesis (PhD)
Keywords: cognitive reserve, ageing, Alzheimer's disease, compensation
Copyright Holders: Copyright 2015 the author
Additional Information:

Chapter 3 appears to be the equivalent of the post-print version of an article published as: Ward, D. D., Summers, M. J., Saunders, N. L., & Vickers, J. C., (2014), Modelling cognitive reserve in healthy middle-aged and older adults: The Tasmanian Healthy Brain Project, International psychogeriatric, 27(4), 579-589. Copyright International Psychogeriatric Association 2014

Chapter 4 appears to be the equivalent of the post-print version of an article published as: Ward, D. D., Summers, M. J., Saunders, N. L., Janssen, P., Stuart, K. E., Vickers, J. C., (2014), APOE and BDNF Val66Met polymorphisms combine to influence episodic memory
function in older adults, Behavioural brain research, 271, 309-315

Date Deposited: 02 Sep 2016 01:49
Last Modified: 02 Sep 2016 01:49
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