Caloric restriction suppresses microglial activation and prevents neuroapoptosis following cortical injury in rats.

ABSTRACT: Traumatic brain injury (TBI) is a widespread cause of death and a major source of adult disability. Subsequent pathological events occurring in the brain after TBI, referred to as secondary injury, continue to damage surrounding tissue resulting in substantial neuronal loss. One of the hallmarks of the secondary injury process is microglial activation resulting in increased cytokine production. Notwithstanding that recent studies demonstrated that caloric restriction (CR) lasting several months prior to an acute TBI exhibits neuroprotective properties, understanding how exactly CR influences secondary injury is still unclear. The goal of the present study was to examine whether CR (50% of daily food intake for 3 months) alleviates the effects of secondary injury on neuronal loss following

SUBMITTER: Loncarevic-Vasiljkovic N 

PROVIDER: S-EPMC3352891 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature