Itoh Tatsuki, Satou Takao, Nishida Shozo, Tsubaki Masahiro, Hashimoto Shigeo, Ito Hiroyuki
Department of Pathology, Kinki University School of Medicine, Okasayyama City, Osaka, Japan.
Neurol Res. 2009 Feb;31(1):103-9. doi: 10.1179/016164108X323771.
Previous reports have demonstrated that some focal brain injuries increase amyloid precursor protein (APP) immunoreactivity in the region surrounding the injury in the cerebral cortex. However, the chronologic changes in APP expression have not been evaluated after traumatic brain injury (TBI).
In this study, we immunohistochemically and biologically investigated chronologic changes in cellular sources and levels of APP production after rat TBI.
In the present report, we show that traumatic brain injury increased the expression of APP in the neuronal perikarya and in damaged dystrophic neurites from 1 to 90 days after injury. Moreover, 7 days after injury, some macrophages/microglia also were co-localized with APP, which was overproduced by the neuronal perikarya and APP-positive dystrophic neurites after injury and then APP were phagocytosed by macrophages/microglia during this phase. However, astroglia did not express APP immunopositivity after brain injury.
These results suggested that long-term overexpression of APP was confirmed by immunohistochemical and biologic technique after TBI. This may be related to the induction of Alzheimer type dementia and it is a very important risk factor for this disease.
先前的报告表明，一些局灶性脑损伤会增加大脑皮质损伤区域周围淀粉样前体蛋白（APP）的免疫反应性。然而，创伤性脑损伤（TBI）后APP表达的时间变化尚未得到评估。
在本研究中，我们通过免疫组织化学和生物学方法研究了大鼠TBI后APP产生的细胞来源和水平的时间变化。
在本报告中，我们表明创伤性脑损伤在损伤后1至90天增加了神经元胞体和受损营养不良性神经突中APP的表达。此外，损伤后7天，一些巨噬细胞/小胶质细胞也与APP共定位，APP在损伤后由神经元胞体和APP阳性营养不良性神经突过度产生，然后在此阶段被巨噬细胞/小胶质细胞吞噬。然而，脑损伤后星形胶质细胞未表达APP免疫阳性。
这些结果表明，TBI后通过免疫组织化学和生物学技术证实了APP的长期过度表达。这可能与阿尔茨海默型痴呆的诱发有关，并且是该疾病的一个非常重要的危险因素。
