[Trial to produce animal model of Alzheimer's disease by continuous infusion of beta-amyloid protein into the rat cerebral ventricle].
To develop an animal model of Alzheimer's disease, we investigated the toxicity of beta-amyloid protein which is a component of senile plaques in Alzheimer's disease. beta-Amyloid was infused into the cerebral ventricle of rats for 14 days using a mini-osmotic pump. The performance of habituation, water maze and passive avoidance tasks in beta-amyloid protein-treated rats was impaired. Choline acetyltransferase activity significantly decreased in the hippocampus both immediately and 2 weeks after cessation of the infusion. However, the learning impairment is recoverable 2 weeks after cessation of the infusion. Both immediately and 2 weeks after cessation of the infusion, glial fibrillary acidic protein immunoreactivity increased. Further, beta-amyloid protein altered the staining of nuclei of cells in the hippocampus only 2 weeks after cessation. These results suggest that beta-amyloid protein damages the central nervous system in vivo, and that this animal could be used as a model of Alzheimer's disease.
Nabeshima
T
T
Department of Neuropsychopharmacology, Nagoya University School of Medicine, Japan.
D000375:Aging; D000544:Alzheimer Disease / Q000473:pathology / Q000503:physiopathology; D016229:Amyloid beta-Peptides; D000818:Animals; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D002799:Cholinergic Fibers; D004195:Disease Models, Animal; D005904:Glial Fibrillary Acidic Protein; D006801:Humans; D051381:Rats
D016229:Amyloid beta-Peptides; D005904:Glial Fibrillary Acidic Protein; D002795:Choline O-Acetyltransferase