Authors: Tatsuki Itoh Takao Satou Shozo Nishida Masahiro Tsubaki Shigeo Hashimoto Hiroyuki Ito
Publish Date: 2009/01/07
Volume: 324, Issue: 1-2, Pages: 191-199
Abstract
We previously demonstrated the increased amyloid precursor protein APP immunoreactivity around the site of damage after traumatic brain injury TBI However the function of APP after TBI has not been evaluated In this study we investigated the effects of direct infusion of an antiAPP antibody into the damaged brain region on cerebral function and morphological changes following TBI in rats Three days after TBI there were many TUNELpositive neurons and astrocytes around the damaged region and a significantly greater number of TUNELpositive cells in the PBS group compared with the antiAPP group found Seven days after TBI there were significantly a greater number of large glial fibrillary acidic proteinpositive cells long elongated projections and microtubuleassociated protein2positive cells around the damaged region in the antiAPP group compared with the PBS group found Seven days after TBI the region of brain damage was significantly smaller and the time to arrival at a platform was significantly shorter in the antiAPP group compared with the PBS group Furthermore after TBI in the antiAPP group the time to arrival at the platform recovered to that observed in uninjured sham operation group rats These data suggest that the overproduction of APP after TBI inhibits astrocyte activity and reduces neural cell survival around the damaged brain region which speculatively may be related to the induction of Alzheimer diseasetype dementia after TBI
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