Authors: Itoh, Tatsuki¹; Satou, Takao²; Nishida, Shozo³; Tsubaki, Masahiro³; Hashimoto, Shigeo⁴; Ito, Hiroyuki¹

Source: Neurological Research, Volume 31, Number 1, February 2009 , pp. 103-109(7)

Publisher: Maney Publishing

Abstract:

Objective: 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).

Methods: In this study, we immunohistochemically and biologically investigated chronologic changes in cellular sources and levels of APP production after rat TBI.

Results: 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.

Discussion: 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.

Keywords: TRAUMATIC BRAIN INJURY; AMYLOID PRECURSOR PROTEIN; APP OVEREXPRESSION; DYSTROPHIC NEURITES; ALZHEIMER'S DISEASE

Document Type: Research Article

DOI: http://dx.doi.org/10.1179/016164108X323771

Affiliations: 1: Department of Pathology, Kinki University School of Medicine, Osaka, Japan 2: Department of Pathology, Kinki University School of Medicine, Osaka, Japan; Division of Hospital Pathology, Hospital of Kinki University School of Medicine, Osaka, Japan; Division of Sports Medicine, Institute of Life Science, Kinki University, Osaka, Japan 3: Kinki University School of Pharmaceutical Sciences, Osaka, Japan 4: Department of Pathology, PL Hospital, Osaka, Japan

Publication date: 2009-02-01

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