TRAUMATIC BRAIN INJURY IN RAT PRODUCES CHANGES OF BETA-AMYLOID PRECURSOR PROTEIN IMMUNOREACTIVITY

beta-AMYLOID precursor protein immunoreactivity (APP) was studied afte r a mild compression contusion trauma to rat parietal cortex. Neurones in the periphery of the cortical lesion, i.e. tissue subjected to she ar stress, showed markedly reduced immunoreactivity 1 and 3 days after injury. Numerous axons in the ipsilateral subcortical white matter an d thalamus became immunoreactive. At 21 days, small rounded profiles a ppeared in the neuropil of the damaged cortex and in the thalamus. Thu s, traumatic brain injury appears to induce several types of APP chang es. The accumulation in neuronal processes is probably caused by distu rbed axonal transport induced by trauma. Since APP is assumed to be ex citoprotective, modulating intracellular Ca2+ responses, the decreased immunoreactivity noticed in the periphery of the lesion may render th e neurones in this region more vulnerable to secondary injury mechanis ms.