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Brain Trauma Induces Massive Hippocampal Neuron Death Linked to a Surge in β-Amyloid Levels in Mice Overexpressing Mutant Amyloid Precursor Protein
Journal article   Open access   Peer reviewed

Brain Trauma Induces Massive Hippocampal Neuron Death Linked to a Surge in β-Amyloid Levels in Mice Overexpressing Mutant Amyloid Precursor Protein

Douglas H Smith, Michio Nakamura, Tracy K McIntosh, Jun Wang, Amarís Rodríguez, Xiao-Han Chen, Ramesh Raghupathi, Kathryn E Saatman, James Clemens, M. Luise Schmidt, …
The American journal of pathology, v 153(3), pp 1005-1010
Sep 1998
PMID: 9736050
url
https://doi.org/10.1016/S0002-9440(10)65643-XView
Published, Version of Record (VoR) Open

Abstract

Regular
Although brain trauma is a risk factor for Alzheimer’s disease, no experimental model has been generated to explore this relationship. We developed a model of brain trauma in transgenic mice that overexpress mutant human amyloid precursor protein (PDAPP) leading to the appearance of Alzheimer’s disease-like β-amyloid (Aβ) plaques beginning at 6 months of age. We induced cortical impact brain injury in the PDAPP animals and their wild-type littermates at 4 months of age, ie, before Aβ plaque formation, and evaluated changes in posttraumatic memory function, histopathology, and regional tissue levels of the Aβ peptides Aβ 1–40 and Aβ 1–42 . We found that noninjured PDAPP mice had impaired memory function compared to noninjured wild-type littermates ( P < 0.01) and that brain-injured PDAPP mice had more profound memory dysfunction than brain-injured wild-type littermates ( P < 0.001). Although no augmentation of Aβ plaque formation was observed in brain-injured PDAPP mice, a substantial exacerbation of neuron death was found in the hippocampus ( P < 0.001) in association with an acute threefold increase in Aβ 1–40 and sevenfold increase in Aβ 1–42 levels selectively in the hippocampus ( P < 0.01). These data suggest a mechanistic link between brain trauma and Aβ levels and the death of neurons.

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Pathology
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