Diffuse neuronal perikaryon amyloid precursor protein immunoreactivity in a focal head impact model

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dc.contributor.authorVan Den Heuvel, C.
dc.contributor.authorLewis, S.
dc.contributor.authorWong, M.
dc.contributor.authorManavis, J.
dc.contributor.authorFinnie, J.
dc.contributor.authorBlumbergs, P.
dc.contributor.authorJones, N.
dc.contributor.authorReilly, P.
dc.contributor.editorMarmarou, A.
dc.contributor.editorBullock, R.
dc.contributor.editorAvezaat, C.
dc.contributor.editorBaethmann, A.
dc.contributor.editorBecker, D.
dc.contributor.editorBrock, M.
dc.contributor.editorHoff, J.
dc.contributor.editorNagai, H.
dc.contributor.editorReulen, H.J.
dc.contributor.editorTeasdale, G.
dc.date.issued1998
dc.description.abstractAmyloid precursor protein (APP) has been shown to accumulate in traumatically injured axons as early as 1 hour after injury. This accumulation may be due to interruption of fast axoplasmic transport and/or upregulation of APP synthesis. The aim of this study was to examine the neuronal cell body response to head impact using APP immunostaining in a focal non-missile head impact model. Ten anaesthetised and ventilated 2 year old Merino ewes were subjected to graded impact in the left temporal region by captive bolt. 2 hours after impact the brain was perfused fixed with formaldehyde. The tissue was mounted in paraffin, sectioned and stained with a monoclonal antibody to APP and standard H&E stain. APP positivity was semi-quantitated using a modification of our previously described sector scoring system [1]. Widespread neuronal APP positivity was found in the cerebral hemispheres and brain stem distant from the site of focal injury in all 10 animals. The most prominent APP positivity was found in the nerve cell bodies of the impacted left cerebral hemisphere. APP positive neurons were also found within regions which were structurally normal when stained with H&E. These results demonstrate diffuse neuronal perikaryon APP immunoreactivity following a focal head impact injury. The expression of APP within the neuronal cell body may be due to upregulation of APP synthesis or alterations in the availability of epitopes of APP. Further studies are in progress to address these hypotheses.
dc.identifier.citationActa Neurochirurgica, Supplement, 1998; 71(SUPPL. 71):209-211
dc.identifier.doi10.1007/978-3-7091-6475-4_60
dc.identifier.issn0065-1419
dc.identifier.orcidVan Den Heuvel, C. [0000-0003-0664-8935]
dc.identifier.orcidManavis, J. [0000-0001-7381-7781] [0000-0003-1268-561X]
dc.identifier.orcidFinnie, J. [0000-0003-2277-1693]
dc.identifier.urihttp://hdl.handle.net/2440/5470
dc.language.isoen
dc.publisherSPRINGER-VERLAG WIEN
dc.source.urihttps://doi.org/10.1007/978-3-7091-6475-4_60
dc.subjectBrain
dc.subjectTemporal Lobe
dc.subjectNeurons
dc.subjectAxons
dc.subjectAnimals
dc.subjectSheep
dc.subjectHead Injuries, Closed
dc.subjectAmyloid beta-Protein Precursor
dc.subjectImmunoenzyme Techniques
dc.subjectFemale
dc.titleDiffuse neuronal perikaryon amyloid precursor protein immunoreactivity in a focal head impact model
dc.typeJournal article
pubs.publication-statusPublished

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