Scamming or cheating people out of money or information, is a public health problem associated with decreased quality of life, functional dependence, and negative health outcomes. Individuals in late middle and old age are at particular risk of scamming, but the reasons why are unclear. Motivated by theories of cognitive, emotional and neural aging, this proposal will investigate potential risk factors contributing to heightened vulnerability to scamming and deceptive situations in middle-aged and older adults. In particular, we will determine the cognitive, affective and neural changes associated with normal aging that contribute to this growing problem.

The perirhinal cortex (PRC) plays an important role in object discrimination and object recognition, two behaviors that allow animals to function within, and navigate through their environment.  Emerging data regarding the impact of aging on the PRC suggests that across species, including rats, monkeys and humans, PRC functions decline with age.  However, little is known regarding the impact of declines in object discrimination on hippocampally-mediated memory that rely on pattern separation computations and high-level associations, both of which are served by the perirhinal cortex (Kent et al, 2016).  Moreover, it is likely that other important real-world functions such as face perception and spatial navigation rely on brain networks that include PRC.  Importantly, recent published studies and data collected by members of the workgroup suggest the postrhinal cortex (POR; also called parahippocampal cortex in primates) remains relatively intact in older adults (de Chastelaine et al., 2016), suggesting that context – scenes and spatial information integrated with objects – may be utilized by older animals and humans in order to compensate for poor object discrimination.  In this project, we will explore age-related changes in function and structure of the PRC, how PRC structure/function relates to hippcampally mediated forms of memory and other real-world tasks, and how scenes and spatial context, mediated by POR might be employed to compensate for age-related changes in memory functioning.

A decline in brain health and associated loss of cognitive function in healthy aging decreases quality of life. Better tools are needed to enhance brain health and improve cognitive performance in healthy brain aging in order to delay, reduce or even reverse healthy brain aging. This proposal is designed to evaluate the pairing of cognitive training with transcutaneous vagal nerve stimulation – the non-invasive neurostimulation technology that has shown promise in increasing neuroplasticity and enhancing cognitive performance.

Longitudinal and cross-sectional studies confirm an association between increasing age and cognitive decline.  Several common health-related factors such as cardiovascular diseases and hypertension (HTN) contribute to age-related changes in cognition. Elevations in blood pressure are highly correlated with increased risk of heart disease, ischemic and hemorrhagic strokes, vascular dementia, Alzheimer’s disease and age-related cognitive decline, with studies showing an association between chronicity of HTN and late-life cognitive deficits. The late-life decrease in cognitive performance is more pronounced when blood pressure is left untreated in middle-age. White-matter hyperintensities (WMH), a known outcome of chronic HTN, has been found to affect cognitive function, but to date there are no therapeutic options to mitigate these lesions. There is growing evidence that other mechanisms independently or in concert with WMH affect cognition, and, importantly, may be treatable. Findings from different lines of inquiry suggest that vascular changes such as loss of microvascular density, or microvascular rarefaction (MVR), may be precursors to hypertension, and others have linked MVR with insulin-like growth factor-1 (IGF-1) deficiencies. Based on both experimental and clinical studies, we propose that among hypertensives these lines of evidence intersect and suggest that age-related decline in IGF-1 concentrations are related to greater microvascular rarefaction and vascular resistance, and therefore late-life cognitive decline. Exercise studies provide an opportunity to begin exploring this premise given the previously demonstrated effects of exercise in attenuating vascular dysfunction, HTN, IGF-1 deficiency, and age-related cognitive decline.

The purpose of this proposal is to study gut-brain interactions in the context of cognitive aging.  Gut health influences cognitive outcomes and alterations in brain health are often accompanied by impaired intestinal functions.  As gut health is likely a modifiable factor mediating cognitive resilience, several potential mechanisms of the bidirectional interactions across the gut-brain axis warrant further investigation.  The ultimate goal of this study is to determine if novel therapeutic strategies targeting the gut can improve age-related cognitive decline in a validated rodent model of aging.