CONTINUOUS-INFUSION OF BETA-AMYLOID PROTEIN INTO THE RAT CEREBRAL VENTRICLE INDUCES LEARNING IMPAIRMENT AND NEURONAL AND MORPHOLOGICAL DEGENERATION

To investigate the toxicity of beta-amyloid protein, a component of th e senile plaques in Alzheimer's disease, it was infused into the cereb ral ventricle of rats for 14 days by a mini-osmotic pump. Performances in the water maze and passive avoidance tasks in beta-amyloid protein -treated rats were impaired. Choline acetyltransferase activity signif icantly decreased in the hippocampus both immediately and 2 weeks afte r the cessation of the infusion. However, the learning impairment was recoverable 2 weeks after cessation of the infusion. Both immediately and 2 weeks after the cessation of the infusion, glial fibrillary acid ic protein immunoreactivity increased. Furthermore, beta-amyloid prote in altered the staining in the nuclei of hippocampal cells for only 2 weeks after the cessation. These results suggest that beta-amyloid pro tein produces some damage in the central nervous system in vivo.