Expression of amyloid precursor protein after rat traumatic brain injury

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.

[1]  T. Satou,et al.  Immature and mature neurons coexist among glial scars after rat traumatic brain injury , 2007, Neurological research.

[2]  S. Wisniewski,et al.  Association of increased cortical soluble abeta42 levels with diffuse plaques after severe brain injury in humans. , 2007, Archives of neurology.

[3]  H. B. Harvey,et al.  Proliferation and neuronal differentiation of mitotically active cells following traumatic brain injury , 2003, Experimental Neurology.

[4]  Wutian Wu,et al.  Potential roles of Alzheimer precursor protein A4 and β‐amyloid in survival and function of aged spinal motor neurons after axonal injury , 2003, Journal of neuroscience research.

[5]  P. Kochanek,et al.  Changes in expression of amyloid precursor protein and interleukin-1beta after experimental traumatic brain injury in rats. , 2002, Journal of neurotrauma.

[6]  R. Colello,et al.  Traumatic brain injury induced cell proliferation in the adult mammalian central nervous system. , 2002, Journal of neurotrauma.

[7]  P. Reilly,et al.  Upregulation of Amyloid Precursor Protein Messenger RNA in Response to Traumatic Brain Injury: An Ovine Head Impact Model , 1999, Experimental Neurology.

[8]  T. Yamaki,et al.  Experimental brain injury induces expression of amyloid precursor protein, which may be related to neuronal loss in the hippocampus. , 1998, Journal of neurotrauma.

[9]  M. Mattson,et al.  Impaired mitochondrial function, oxidative stress and altered antioxidant enzyme activities following traumatic spinal cord injury , 1997, Brain Research.

[10]  K. Marder,et al.  Alzheimer's disease after remote head injury: an incidence study. , 1997, Journal of neurology, neurosurgery, and psychiatry.

[11]  C. Lee,et al.  Mitochondrial dysfunction and calcium perturbation induced by traumatic brain injury. , 1997, Journal of neurotrauma.

[12]  Y. Olsson,et al.  Changes in microtubule-associated protein 2 and amyloid precursor protein immunoreactivity following traumatic brain injury in rat: influence of MK-801 treatment , 1996, Brain Research.

[13]  D. Hovda,et al.  Lactate accumulation following concussive brain injury: the role of ionic fluxes induced by excitatory amino acids , 1995, Brain Research.

[14]  D. Graham,et al.  Apolipoprotein E ε4 allele is associated with deposition of amyloid β-protein following head injury , 1995, Nature Medicine.

[15]  D. Graham,et al.  Apolipoprotein E epsilon 4 allele is associated with deposition of amyloid beta-protein following head injury. , 1995, Nature medicine.

[16]  R. Hayes,et al.  Neurofilament 68 and neurofilament 200 protein levels decrease after traumatic brain injury. , 1994, Journal of neurotrauma.

[17]  L. Murray,et al.  Beta amyloid protein deposition in the brain after severe head injury: implications for the pathogenesis of Alzheimer's disease. , 1994, Journal of neurology, neurosurgery, and psychiatry.

[18]  D. Stephenson,et al.  Amyloid precursor protein accumulates in regions of neurodegeneration following focal cerebral ischemia in the rat , 1992, Brain Research.

[19]  M. Takeda,et al.  Amyloid β-protein precursor deposition in rat hippocampus lesioned by ibotenic acid injection , 1992, Neuroscience Letters.

[20]  D. Selkoe,et al.  Processing of the amyloid protein precursor to potentially amyloidogenic derivatives. , 1992, Science.

[21]  R. Hayes,et al.  Microtubule-associated protein 2 levels decrease in hippocampus following traumatic brain injury. , 1992, Journal of neurotrauma.

[22]  N. Otsuka,et al.  Rapid appearance of β-amyloid precursor protein immunoreactivity in damaged axons and reactive glial cells in rat brain following needle stab injury , 1991, Brain Research.

[23]  D. Allsop,et al.  The occult aftermath of boxing. , 1990, Journal of neurology, neurosurgery, and psychiatry.

[24]  D. Price,et al.  Precursor of amyloid protein in Alzheimer disease undergoes fast anterograde axonal transport. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[25]  G. Heinrich.  Amyloid A4 protein and its precursor in Down's syndrome and Alzheimer's disease. , 1989, The New England journal of medicine.

[26]  G. W. Roberts.  IMMUNOCYTOCHEMISTRY OF NEUROFIBRILLARY TANGLES IN DEMENTIA PUGILISTICA AND ALZHEIMER'S DISEASE: EVIDENCE FOR COMMON GENESIS , 1988, The Lancet.

[27]  H. Wiśniewski,et al.  Molecular cloning and characterization of a cDNA encoding the cerebrovascular and the neuritic plaque amyloid peptides. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[28]  M. Lerman,et al.  Characterization and chromosomal localization of a cDNA encoding brain amyloid of Alzheimer's disease. , 1987, Science.

[29]  D. Selkoe,et al.  Isolation of Low‐Molecular‐Weight Proteins from Amyloid Plaque Fibers in Alzheimer's Disease , 1986, Journal of neurochemistry.

[30]  R. Martins,et al.  Neuronal origin of a cerebral amyloid: neurofibrillary tangles of Alzheimer's disease contain the same protein as the amyloid of plaque cores and blood vessels. , 1985, The EMBO journal.