Neurophysiological changes associated with cognitive training in older adults 'at risk' for dementia: application of the mismatch negativity event-related potential
thesisposted on 2022-03-29, 00:25 authored by Loren Mowszowski
Background: The prevalence of dementia worldwide is expected to increase dramatically with the rapidly expanding ageing population. Research has identified sub-groups of older people with increased risk of dementia, including those with subjective cognitive impairment, depression and mild cognitive impairment. With the current lack of effective treatments for dementia, secondary prevention approaches targeting 'at risk' older individuals are warranted. It has been suggested that cognitive training may have the capacity to delay or slow cognitive decline in these 'at risk' groups. However, the extent to which such interventions also have the capacity to alter underlying brain functioning is largely unknown. -- Aims: This body of research aimed to: 1) examine whether cognitive training may be a viable early intervention strategy for 'at risk' older adults; 2) determine whether utilisation of neurophysiological paradigms may be a viable way to probe underlying brain dysfunction in 'at risk' groups; and 3) investigate the extent to which cognitive training may be associated with altered neurophysiological responses. -- Methods: The first aim of this thesis was achieved with the publication of a literature review exploring evidence for the efficacy of cognitive training. The second aim of this research employed an event-related potential Mismatch Negativity (MMN) paradigm to determine the capacity to detect changes in 'pre-attentive' cognitive processes in 'at risk' groups, which in turn, are thought to recruit distinct neurobiological circuits. Finally, using a randomised controlled trial in 40 'at risk' older people, this research examined the capacity for cognitive training to alter the MMN response. -- Results: The findings of this research confirmed that cognitive training does offer promise as a secondary prevention tool for cognitive decline in 'at risk' cohorts. It also showed that the MMN response is reduced in 'at risk' groups relative to healthy older controls and is also associated with neuropsychological and psychosocial functioning, suggesting its utility as a neural marker of brain dysfunction. Finally, results showed that this marker is enhanced following cognitive training, supporting the notion that neuroplastic changes do occur in relation to this non-pharmacological intervention. -- Implications: Further research exploring the relationship between the MMN marker and underlying pathophysiological brain changes associated with dementia is now warranted, as well as research exploring the capacity of this marker to predict cognitive decline longitudinally.