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"Won't you be my neighbor?": deciphering the mechanisms of neuroprotection induced by social interaction.

See related article, pages 3606–3611.

Accumulating evidence from numerous epidemiological and preclinical studies has suggested that social factors can have a profound influence on physical and mental health.1–7 People with high levels of social support or large social networks exhibit lower all-cause mortality and more rapid and extensive functional and cognitive recovery after a wide variety of pathological insults, including stroke.1–6 In contrast, social isolation is associated with increased mortality and morbidity in patients with established vascular disease.2,4 Individuals who report lack of social support or isolation have an increased incidence of recurrent stroke, poorer recovery, and greater functional decline over the 5 years following a stroke compared with individuals with social support.3 Low social support is associated with increased vascular risk even after controlling for common risk factors such as age, education, obesity, exercise, smoking, and drinking.2,3 Attesting to the importance of behavioral factors in stroke outcome is that these same effects can be modeled in animals.5 Social interaction improves behavioral deficits and reduces histological damage after experimental stroke, whereas isolation, even for as little as a week, enhances ischemic damage.1,5 The work by Karelina et al in this issue of Stroke moves us closer to understanding the basic mechanisms involved in the protective effects of social interaction.

Social isolation has been defined in a myriad of ways in the literature. In general, in population-based studies, social isolation represents people who had poor (less than 3 people well enough to visit home) or limited primary informal social networks that include friend, family, or friend-neighbors.2–4,6 In animal studies, pair-housing …