Considerable evidence from clinical studies has shown that outcomes after stroke are strongly influenced by psychosocial factors. Patients with high levels of social support or large social networks exhibit more rapid and extensive functional recovery after stroke than socially isolated individuals. In contrast, perceived social isolation predicts morbidity and mortality from cerebrovascular disease. These same effects can be reproducibly demonstrated in animals;social interaction improves behavioral deficits and reduces histological damage after experimental stroke, whereas social isolation enhances ischemic damage. The mechanisms that mediate the interactions between the social environment, behavioral responses, and disease outcomes remain unclear. Advancing age is associated with an increased risk for the development of many chronic diseases including cerebrovascular disease. With our aging population, the incidence and prevalence of stroke will continue to rise, leading to increasing numbers of stroke survivors in our communities. Many older individuals are exposed to significant psychosocial stress and isolation (loss of spouse, depression, frailty etc.), however no studies have investigated the mechanisms by which psychosocial factors influence behavioral and outcomes in aged animals. We will utilize a transient focal ischemia model in socially isolated and pair housed males. We will examine the contribution of aging to the detrimental effects of isolation on the amount of stroke damage, the immune response, and behavioral recovery. Components of the peripheral and central immune system will be examined and manipulated.
Stroke is now the leading cause of disability in the United States. Social isolation predicts morbidity and mortality from cerebrovascular disease. The mechanisms that mediate the interactions between the social environment, behavioral responses, and disease outcomes will be studied in a rodent model.
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