Social Interaction Improves Experimental Stroke Outcome

Craft, Tara K.S.; Glasper, Erica R.; McCullough, Louise D.; Zhang, Ning; Sugo, Nobuo; Otsuka, Takashi; Hurn, Patricia D.; DeVries, A. Courtney

doi:10.1161/01.str.0000177538.17687.54

Cited by 72 publications

(93 citation statements)

References 40 publications

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“…1). These data confirm and extend previous reports that social isolation potentiates the pathophysiological response to ischemia (8,9) and suggest that social isolation contributes to early differences in the trajectory of ischemic injury development.…”

Section: Discussionsupporting

confidence: 91%

“…However, both social isolation and perceived lack of social support are predictive of disease outcome independent of health behaviors (6,7). Furthermore, the negative effects of social isolation on stroke and cardiac arrest outcome can be reproduced in mice, and the data suggest that socially isolated and socially housed mice mount a quantitatively different pathophysiological response to ischemic damage (8,9).…”

mentioning

confidence: 99%

“…Importantly, emerging evidence indicates a relationship between the social environment and systemic inflammation (16,17), and in otherwise healthy humans, low social integration is associated with increased CRP concentrations (18,19). Further, socially isolated mice exhibit increased intraischemic serum CRP concentrations relative to socially housed animals after experimental stroke (8). Although a direct causative role for CRP on the extent of ischemic injury has not been established, both the clinical (11,(16)(17)(18) and animal (8) data provide evidence of a strong correlation between social factors and the inflammatory response typically associated with ischemic injury.…”

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confidence: 99%

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Social isolation alters neuroinflammatory response to stroke

Karelina¹,

Norman²,

Zhang³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Social isolation has dramatic long-term physiological and psychological consequences; however, the mechanisms by which social isolation influences disease outcome are largely unknown. The purpose of the present study was to investigate the effects of social isolation on neuronal damage, neuroinflammation, and functional outcome after focal cerebral ischemia. Male mice were socially isolated (housed individually) or pair housed with an ovariectomized female before induction of stroke, via transient intraluminal middle cerebral artery occlusion (MCAO), or SHAM surgery. In these experiments, peri-ischemic social isolation decreases poststroke survival rate and exacerbates infarct size and edema development. The social influence on ischemic damage is accompanied by an altered neuroinflammatory response; specifically, central interleukin-6 (IL-6) signaling is down-regulated, whereas peripheral IL-6 is up-regulated, in isolated relative to socially housed mice. In addition, intracerebroventricular injection of an IL-6 neutralizing antibody (10 ng) eliminates social housing differences in measures of ischemic outcome. Taken together, these data suggest that central IL-6 is an important mediator of social influences on stroke outcome.focal cerebral ischemia ͉ neuroinflammation

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Section: Discussionsupporting

confidence: 91%

mentioning

confidence: 99%

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confidence: 99%

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Social isolation alters neuroinflammatory response to stroke

Karelina¹,

Norman²,

Zhang³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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104

116

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“…The mechanism underlying the effects of stress on stroke outcome likely involves corticosterone acting through GR to increase subsequent ischemia-induced neuronal death (Craft et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Stress Increases Vulnerability to Inflammation in the Rat Prefrontal Cortex

Pablos¹,

Villarán²,

Argüelles³

et al. 2006

J. Neurosci.

193

176

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Inflammation could be involved in some neurodegenerative disorders that accompany signs of inflammation. However, because sensitivity to inflammation is not equal in all brain structures, a direct relationship is not clear. Our aim was to test whether some physiological circumstances, such as stress, could enhance susceptibility to inflammation in the prefrontal cortex (PFC), which shows a relative resistance to inflammation. PFC is important in many brain functions and is a target for some neurodegenerative diseases. We induced an inflammatory process by a single intracortical injection of 2 g of lipopolysaccharide (LPS), a potent proinflammogen, in nonstressed and stressed rats. We evaluated the effect of our treatment on inflammatory markers, neuronal populations, BDNF expression, and behavior of several mitogen-activated protein (MAP) kinases and the transcription factor cAMP response element-binding protein. Stress strengthens the changes induced by LPS injection: microglial activation and proliferation with an increase in the levels of the proinflammatory cytokine tumor necrosis factor-␣; loss of cells such as astroglia, seen as loss of glial fibrillary acidic protein immunoreactivity, and neurons, studied by neuronal-specific nuclear protein immunohistochemistry and GAD67 and NMDA receptor 1A mRNAs expression by in situ hybridization. A significant increase in the BDNF mRNA expression and modifications in the levels of MAP kinase phosphorylation were also found. In addition, we observed a protective effect from RU486 [mifepristone (11␤-[p-(dimethylamino)phenyl]-17␤-hydroxy-17-(1-propynyl)estra-4,9-dien-3-one)], a potent inhibitor of the glucocorticoid receptor activation. All of these data show a synergistic effect between inflammation and stress, which could explain the relationship described between stress and some neurodegenerative pathologies.

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“…This finding might reflect incomplete spontaneous recovery in some patients at the time of study entry (supported by the inverse relation between time after stroke and gains to week 4), overcoming of learned disuse, effects of repeated testing, or direct psychosocial effects of study participation. 25 Second, outside therapy was common among subjects in both treatment arms. Although the amount of such therapy had little relation to outcomes in the current study, experience is nonetheless important in shaping outcome after stroke and in enabling restorative therapies, 26 and might therefore be important in other studies.…”

Section: Discussionmentioning

confidence: 99%

Randomized, Placebo-Controlled, Double-Blind Study of Ropinirole in Chronic Stroke

Cramer

Dobkin

Noser

et al. 2009

Stroke

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Background and Purpose-Evidence suggests the potential to improve motor status in patients with stroke by modifying brain catecholaminergic tone. The current study hypothesized that increased dopaminergic tone via the dopamine agonist ropinirole, when combined with physiotherapy (PT), would significantly and safely increase gait velocity. Methods-Patients with moderate motor deficits due to stroke 1 to 12 months prior were randomized (double blinded) to 9 weeks of immediate-release ropinirole or placebo, each with PT, and followed up for 3 additional weeks. Drug dose (0.25 to 4 mg once daily) was titrated weekly, as tolerated. The primary end point was gait velocity during the 12 weeks of study participation. Results-Patients in the ropiniroleϩPT group averaged 2.4 mg/d by end of week 9, although the target dose was at least 3 mg/d. RopiniroleϩPT was generally safe and well tolerated, including no drug-related serious adverse events. Across all 33 enrollees, significant gains were found over time for gait velocity and for most secondary end points. However, gains did not differ by treatment assignment. PT and occupational therapy were commonly prescribed outside of the trial, although the extent of these was not correlated with study outcomes. Conclusions-At doses achieved in this trial, increased dopaminergic tone via ropiniroleϩPT was generally well tolerated but did not show any improvement over and above the effects of PT alone.

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Social Interaction Improves Experimental Stroke Outcome

Cited by 72 publications

References 40 publications

Social isolation alters neuroinflammatory response to stroke

Social isolation alters neuroinflammatory response to stroke

Stress Increases Vulnerability to Inflammation in the Rat Prefrontal Cortex

Randomized, Placebo-Controlled, Double-Blind Study of Ropinirole in Chronic Stroke

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