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    Characterisation of the effect of knockout of the amyloid precursor protein on outcome following mild traumatic brain injury

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    Author
    Corrigan, F; Vink, R; Blumbergs, PC; Masters, CL; Cappai, R; van den Heuvel, C
    Date
    2012-04-27
    Source Title
    BRAIN RESEARCH
    Publisher
    ELSEVIER
    University of Melbourne Author/s
    Masters, Colin; Cappai, Roberto
    Affiliation
    Pathology
    Metadata
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    Document Type
    Journal Article
    Citations
    Corrigan, F., Vink, R., Blumbergs, P. C., Masters, C. L., Cappai, R. & van den Heuvel, C. (2012). Characterisation of the effect of knockout of the amyloid precursor protein on outcome following mild traumatic brain injury. BRAIN RESEARCH, 1451, pp.87-99. https://doi.org/10.1016/j.brainres.2012.02.045.
    Access Status
    This item is currently not available from this repository
    URI
    http://hdl.handle.net/11343/33319
    DOI
    10.1016/j.brainres.2012.02.045
    Description

    C1 - Journal Articles Refereed

    Abstract
    The amyloid precursor protein (APP) increases following traumatic brain injury (TBI), although the functional significance of this remains unclear largely because the functions of the subsequent APP metabolites are so different: Aβ is neurotoxic whilst sAPPα is neuroprotective. To investigate this further, APP wildtype and knockout mice were subjected to mild diffuse TBI and their outcomes compared. APP knockout mice displayed significantly worse cognitive and motor deficits, as demonstrated by the Barnes Maze and rotarod respectively, than APP wildtype mice. This was associated with a significant increase in hippocampal and cortical cell loss, as well as axonal injury, in APP knockout mice and an impaired neuroreparative response as indicated by diminished GAP-43 immunoreactivity when compared to APP wildtype mice. This study is the first to demonstrate that endogenous APP is beneficial following mild TBI, suggesting that the upregulation of APP observed following injury is an acute protective response.
    Keywords
    Central Nervous System; Nervous System and Disorders

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