This thesis focused on changes in memory-related functional brain activation patterns in healthy ageing and Alzheimer's disease (AD) in order to gain a better understanding of the neural mechanisms that underlie successful memory strategies.
Such information is needed in order to devise more effective cognitive intervention programmes aimed at enhancing memory function.
Current literature on brain activation changes in associative memory processes in healthy ageing and AD was reviewed and linked to results from behavioural studies that investigated different memory-enhancing learning strategies. It was
suggested that semantic processing is a key aspect of improving memory in both healthy ageing and AD, and that rehabilitation strategies should target residual memory function in AD.
A second literature review explored how functional magnetic resonance imaging (fMRJ) might be applied to measure treatment effects and brain plasticity in cognitive intervention aimed at people with AD. Paradigms on face-name learning in fMRI in healthy ageing, mild cognitive impairment, and AD were reviewed, and recommendations for a novel face-name learning task were made.
Study 1 compared brain activity in healthy young and older adults during a face-name learning paradigm. Results suggested that the observed hyper-activation in the older group may reflect increased effort to attain task performance similar to that of the young group.
In Study 2, brain activation during face-name learning was compared between healthy older adults and people with AD. The AD group showed hyper-activation compared to the healthy older group in posterior parietal areas during recognition. This may be an indicator of inefficient inhibition.
Study 3 compared brain activation differences in a small group of people with AD prior to and following an eight-week cognitive rehabilitation intervention. Small improvements in immediate recognition were observed. Brain activation was generally higher prior to than following treatment, which may mean more efficient inhibition of default mode network regions following treatment.