Affiliations: [a] Department of Behavioral Science, University of Kentucky, Lexington, KY, USA
| [b] Department of Psychiatry, University of California, San Francisco, CA, USA
| [c] Movement Disorders Program, Medical University of South Carolina, Charleston, SC, USA
| [d] Department of Gerontology, University of Maryland, Baltimore, MD, USA
| [e] Department of Neurology, University of Kentucky, Lexington, KY, USA
| [f] Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA
Correspondence:
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Correspondence to: Lucas Broster, MD/PhD, Department of Behavioral Science, Aging Brain and Cognition Laboratory, 116 Medical Behavioral Science Building, University of Kentucky, Lexington, KY 40536-0086, USA. Tel.: +1 859 338 0095; E-mail: lukebroster@gmail.com.
Abstract: Emotional enhancement effects on memory have been reported to mitigate the pathophysiology of Alzheimer’s disease (AD). However, relative to their manifestation in persons without pathologic aging, these effects may be reduced in magnitude or even deleterious, especially in tasks that more closely model ecologic memory performance. Based upon a synthesis of such reports, we hypothesized that in persons with AD low arousal positive stimuli would evoke relatively intact emotional enhancement effects, but that high arousal negative stimuli would evoke disordered emotional enhancement effects. To assess this, participants with and without mild cognitive impairment (MCI) presumed to be due to AD performed an emotionally-valenced short-term memory task while encephalography was recorded. Results indicated that for persons with MCI, high arousal negative stimuli led to working memory processing patterns previously associated with MCI presumed due to AD and dementia of the Alzheimer-type. In contrast, low arousal positive stimuli evoked a processing pattern similar to MCI participants’ unaffected spouses. Our current findings suggest that low arousal positive stimuli attenuate working memory deficits of MCI due to AD.
