Exposure to chronic stressors ? that is, demanding life situations that persist for long periods of time ?accelerates the aging of the immune system. Termed immunosenescence, this immune aging is marked by increasingly altered T cell numbers and activity and elevated markers of inflammation. Our long-term objective is to identify appropriate therapeutic targets for older adults to reduce the psycho-immunological burden of chronic stress. Recent models of stress adaptation and neurobiological regulation suggest that similar neural structures and networks support cognition, the autonomic nervous system (ANS) and emotion regulation, each of which are important for physiological and emotional adaptation to stressors. For older adults, a combination of aging- and chronic stress-related neurological changes may compromise the regulation of these domains, thereby reducing stress adaptation capacity and increasing susceptibility to accelerated immunosenescence. Our current objective is to examine the role of cognitive function in adaptive capacity and stress-related immune alterations that signal immunosenescence. Our central hypothesis is that cognitive decline will accelerate immunosenescence in older adults exposed to chronic stressors, insofar as such decline reflects an overall reduction in adaptive capacity ? that is, the capacity to respond flexibly and adaptively to environmental challenges. We propose to test this hypothesis in older caregivers of a family member with Alzheimer?s Disease (AD) or AD-related dementia (ADRD), a population at high risk for stress-associated immune aging.
We aim to directly probe the role of cognitive contributions to adaptive capacity and immunosenescence by using a cognitive training program shown previously to improve so-called fluid cognitive abilities, particular processing speed and attention, in healthy older adults. Importantly, this training also led to better emotional well-being in older adults. A longitudinal design will afford repeated assessments of fluid cognitive abilities, ANS responses and emotion regulation, general emotional well-being and immune markers (inflammatory cytokines and T-cell markers), and analyses of mediational effects. Specifically, AD/ADRD family caregivers will be randomly assigned to engage in home-based, computerized cognitive training, or to a no-training control group. We will then examine the ensuing cognitive, psychophysiological, emotional and immunological changes that occur over a 12-month period.
Our aims are to: (1) identify effects of cognitive training on caregivers? cognitive, autonomic and emotion markers of adaptive capacity (2) identify effects of cognitive training on caregivers? inflammatory cytokine levels and markers of T cell senescence, and (3) determine cognitive, autonomic, and emotion-related mediators of cognitive training effects on immune outcomes. The work proposed here is expected to identify mechanisms involved in older adults? poor emotional well-being and immunosenescence arising from caregiving stress. This identification will afford insight into new intervention targets, like cognitive training, to promote AD caregivers? health and well-being.
Older caregivers of a spouse with dementia experience significantly compromised immune function and increases in inflammation, substantially increasing risk for poor health and early death. This project seeks to identify the cognitive, physiological and emotion mechanisms that may work together to contribute to these immune changes in caregivers. Understanding the multiple, integrative factors that influence caregivers' immune outcomes can help promote interventions that reduce the considerable health risks and health care costs associated with dementia caregiving