Response Inhibition-Related Beta Power: Distinguishing Cognitively Intact Elders by Risk for Alzheimer’s Disease
Date of Award
Master of Science (MS)
Nielson, Kristy A.
Current neuropsychological research demonstrates an association between the Apolipoprotein-E 4 allele (APOE 4) and poorer cognitive outcomes in older adults. However, there is a general lack of consensus regarding the effect the 4 allele has on executive functioning in cognitively intact older adults, and there is even less study of the effects the 4 allele has on specific executive function processes, such as response inhibition. While behavioral task performance may lack the sensitivity to detect subtle differences in cognitively intact, at-risk individuals, neural activity may better differentiate between individuals who are more likely to develop Alzheimer’s disease (AD). Compensatory theories of aging posit at-risk individuals may employ compensatory mechanisms in the form of bilateral neural recruitment and greater frontal activation. While electrophysiological methods, such as ERP and EEG, have been employed to investigate neural activity related to the 4 allele, few studies have examined the differences in these neural markers between cognitively intact older adult carriers and non-carriers. The present study examined EEG oscillatory activity as a biomarker to target these gaps in the existing literature by investigating event-related beta activity in cognitively intact 4 carriers (n = 21) and non-carriers (n = 23) during a response inhibition task. Our findings support compensatory theories of aging by demonstrating cognitively intact older adults employ compensatory mechanisms in the form of bilateral recruitment and greater frontal recruitment specifically during a task requiring inhibitory control. Additionally, these compensatory mechanisms are even greater in individuals at greater risk for developing AD. Results underscore the utility of assessing task-related neural activation during executive function tasks so as to better differentiate individuals at an increased risk for future cognitive impairment. The present study further demonstrates that EEG oscillatory activity, and more specifically beta band activity, may be a useful prodromal marker of cognitive decline.