( from the application): We have established a behaviorally and immunologically sophisticated animal model for the concepts being tested in Projects 1 and 2. Our goal is to identify the specific mechanisms and causal pathways through which social isolation and disruption, in interaction with personality, increases risk for specific infectious, malignant and inflammatory diseases at the end of the life span. We hypothesize that risk for age-associated clinical disease increases when an individual?s social environment is not optimal for that particular individual. We will verify that vulnerability to social isolation is a stable individual trait. We will evaluate the roles of three different mechanisms mediating vulnerability to social isolation and risk for accelerated aging and disease (a) differential exposure to isolation during puberty (b) state and trait differences in adrenal and gonadal function and differential recovery in response to threat. We will identify the active social signals that physiologically ameliorate the negative health effects of social isolation in those individuals that are not predisposed to living alone. Finally, we will identify the physiological consequences of social isolation and disruption by measuring (a) adrenal and reproductive steroids mediating their effects, and (b) the specific molecular and cellular mechanisms by which social isolation and disruption impair the innate immune response (proinflammatory cytokines and natural killer cells).
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