Increased apoptotic neuronal cell death and cognit

Authors: Tatsuki Itoh Motohiro Imano Shozo Nishida Masahiro Tsubaki Nobuyuki Mizuguchi Shigeo Hashimoto Akihiko Ito Takao Satou

Publish Date: 2012/02/29

Volume: 218, Issue: 1, Pages: 209-220

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Abstract

Progressive ageassociated increases in cerebral dysfunction have been shown to occur following traumatic brain injury TBI Moreover levels of neuronal mitochondrial antioxidant enzymes in the aged brain are reduced resulting in free radicalinduced cell death It was hypothesized that cognitive impairment after TBI in the aged progresses to a greater degree than in younger individuals and that damage involves neuronal degeneration and death by free radicals In this study we investigated the effects of free radicals on neuronal degeneration cell death and cognitive impairment in 10weekold young group and 24monthold rats aged group subjected to TBI Young and aged rats received TBI with a pneumatic controlled injury device At 1 3 and 7 days after TBI immunohistochemistry lipid peroxidation and behavioral studies were performed At 1 3 and 7 days postTBI the number of 8hydroxy2′deoxyguanosine 4hydroxy2nonenal and singlestranded DNA ssDNApositive cells and the levels of malondialdehyde around the damaged area after TBI significantly increased in the aged group when compared with the young group P  005 In addition the majority of ssDNApositive cells in both groups colocalized with neuronal cells around the damaged area There was a significant decrease in the number of surviving neurons and an increase in cognitive impairment after TBI in the aged group when compared with the young group P  005 These results indicate that following TBI high levels of free radicals are produced in the aged rat brain which induces neuronal degeneration and apoptotic cell death around the damaged area resulting in cognitive impairment

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