Age and energy intake interact to modify cell stress pathways and stroke outcome.

作者: Thiruma V. Arumugam , Terry M. Phillips , Aiwu Cheng , Christopher H. Morrell , Mark P. Mattson

DOI: 10.1002/ANA.21798

关键词:

摘要: Age and excessive energy intake/obesity are risk factors for cerebrovascular disease, but it is not known if how these affect the extent of brain damage outcome in ischemic stroke. We therefore determined interactions age intake on injury, elucidated underlying mechanisms.We utilized a novel microchip-based immunoaffinity capillary electrophoresis technology to measure panel neurotrophic factors, cytokines cellular stress resistance proteins tissue samples from young, middle old mice that had been maintained control or restricted diets prior cerebral artery occlusion reperfusion (I/R).Mortality focal stroke was increased with advancing reduced by an intermittent fasting (IF) diet. Brain functional impairment were IF young mice, mice. The basal post-stroke levels (BDNF bFGF), protein chaperones (HSP70 GRP78) antioxidant enzyme HO-1 decreased, while inflammatory cortex striatum compared younger coordinately protective decreases mice.Reduction dietary differentially modulates pathways protect neurons against beneficial effects compromised during aging resulting poorer outcome. Ann Neurol 2009.

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