The impact of resilience on healthy aging with multiple sclerosis.

PURPOSE: The aim of this study was to identify characteristics of older persons with multiple sclerosis (MS) reporting high and low levels of resilience. We also examined the influence of resilience on three key elements of healthy aging: level of disability, participation and health-related quality of life (HRQoL). METHODS: Data were extracted from the Canadian Survey of Health, Lifestyle and Aging with MS (n = 743). Lifestyle, psychological health, and quality of life variables were compared between people with high and low resilience scores controlling for confounding variables. We used hierarchical regression to determine the unique contribution of resilience and related variables to healthy aging. RESULTS: Roughly, 1 in 5 respondents reported high resilience (18.8%), while 1 in 3 reported low resilience (33.9%). The group having higher resilience scores lived with less disability (~ 10%) and fatigue, reported greater participation, exercised more, consumed a healthier diet and lived with greater social support and financial security, compared to the lower scoring group. Resilience added only 1-2% of predictive value explaining disability, participation and HRQoL when confounding variables were accounted for. Years since diagnosis, type of MS, depression, fatigue and resilience significantly predicted healthy aging. CONCLUSION: Resilience contributed minimally (but significantly) to healthy aging. Older participants scoring higher on resilience reported healthier lifestyle behaviors (more exercise, better diet) and social/financial support compared to lower scoring respondents. Our findings suggest that self-management programs for older persons with MS should focus on three key factors to foster healthy aging: depression, fatigue and resilience.

Enriched environment enhances transplanted subventricular zone stem cell migration and functional recovery after stroke.

Stroke patients suffer from severe impairments and significant effort is under way to develop therapies to improve functional recovery. Stem cells provide a promising form of therapy to replace neuronal circuits lost to injury. Indeed, previous studies have shown that a variety of stem cell types can provide some functional recovery in animal models of stroke. However, it is unlikely that replacement therapy alone will be sufficient to maximize recovery. The aim of the present study was to determine if rodent stem cell transplants combined with rehabilitation resulted in enhanced functional recovery after focal ischemia in rats. Middle cerebral artery occlusion was induced by injection of the vasoconstrictive peptide endothelin-1 adjacent to the middle cerebral artery. Seven days after stroke the rats received adult neural stem cell transplants isolated from mouse subventricular zone or vehicle injection and then subsequently were housed in enriched or standard conditions. The rats in the enriched housing also had access to running wheels once a week. Enriched housing and voluntary running exercise enhanced migration of transplanted stem cells toward the region of injury after stroke and there was a trend toward increased survival of stem cells. Enrichment also increased the number of endogenous progenitor cells in the subventricular zone of transplanted animals. Finally, functional recovery measured in the cylinder test was facilitated only when the stem cell transplants were combined with enrichment and running exercise 7 days after the transplant. These results suggest that the ability of transplanted stem cells in promoting recovery can be augmented by environmental factors such as rehabilitation.

Endurance exercise regimens induce differential effects on brain-derived neurotrophic factor, synapsin-I and insulin-like growth factor I after focal ischemia.

The optimal amount of endurance exercise required to elevate proteins involved in neuroplasticity during stroke rehabilitation is not known. This study compared the effects of varying intensities and durations of endurance exercise using both motorized and voluntary running wheels after endothelin-I-induced focal ischemia in rats. Hippocampal levels of brain-derived neurotrophic factor, insulin-like growth factor I and synapsin-I were elevated in the ischemic hemisphere even in sedentary animals suggesting an intrinsic restorative response 2 weeks after ischemia. In the sensorimotor cortex and the hippocampus of the intact hemisphere, one episode of moderate walking exercise, but not more intense running, resulted in the greatest increases in levels of brain-derived neurotrophic factor and synapsin-I. Exercise did not increase brain-derived neurotrophic factor, insulin-like growth factor I or synapsin-I in the ischemic hemisphere. In voluntary running animals, both brain and serum insulin-like growth factor I appeared to be intensity dependent and were associated with decreasing serum levels of insulin-like growth factor I and increasing hippocampal levels of insulin-like growth factor I in the ischemic hemisphere. This supports the notion that exercise facilitates the movement of insulin-like growth factor I across the blood-brain barrier. Serum corticosterone levels were elevated by all exercise regimens and were highest in rats exposed to motorized running of greater speed or duration. The elevation of corticosterone did not seem to alter the expression of the proteins measured, however, graduated exercise protocols may be indicated early after stroke. These findings suggest that relatively modest exercise intervention can increase proteins involved in synaptic plasticity in areas of the brain that likely subserve motor relearning after stroke.