Date of Award

Spring 2018

Document Type

Thesis

Degree Name

Master of Science (MS)

Department

Clinical Psychology

First Advisor

Nielson, Kristy A.

Second Advisor

Gordon, Nakia

Third Advisor

Porcelli, Anthony

Abstract

Current ERP research emphasizes age- and pathology-related declines in neural processing in the form of attenuated amplitudes and prolonged latencies. Notably, there is a gap in the ERP literature regarding neural processing trajectories in the time between healthy young adulthood and clinical MCI/AD samples. fMRI research, however, has demonstrated periods of increased, compensatory activation in healthy, cognitively intact APOE ɛ4 carriers both during resting state and event-related tasks (Bondi, Houston, Eyler, & Brown, 2005; Evans et al., 2014; Filippini et al., 2009; Rao et al., 2015), consistent with compensatory theories of cognitive aging (Cabeza, 2002; Park & Reuter-Lorenz, 2009; Reuter-Lorenz & Park, 2014). Such theories suggest increased magnitude and extent of activation in older adults and groups that are at risk for pathological aging (e.g. via APOE ɛ4 allele) to allow for comparable behavioral performance in spite of neural degradation. The current study sought to expand upon the neuroimaging literature by investigating the N200 and N400 components at left and right hemisphere sites between not only healthy young (n = 42) and older adults (total n = 46), but also healthy, cognitively intact older adults with and without genetic risk for AD via the APOE ɛ4 allele (ɛ4+ n = 23, ɛ4- n = 23). Notably, we employed a high-accuracy, low-effort semantic memory task (Famous Names Discrimination Task (FNDT)) for which performance was comparable across groups. Our findings support compensatory theories of cognitive aging by demonstrating larger N400 components, shorter frontal N200 and parietal N400 latencies in older compared to younger adults. Further, we expand upon the pathological aging literature by demonstrating shorter, larger, and more bilaterally comparable ERPs in the ɛ4+ compared to ɛ4- group. Together these results further elucidate the compensatory mechanisms associated with age- and pathology-related cognitive decline in a healthy, cognitively intact sample, and suggest the utility of the FNDT as a potential biomarker for AD risk.

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