Trial to produce animal model of Alzheimer's disease by continuous infusion of β-amyloid protein into the rat cerebral ventricle

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Abstract

To develop an animal model of Alzheimer's disease, we investigated the toxicity of β-amyloid protein which is a component of senile plaques in Alzheimer's disease. β-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 β-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, β- amyloid protein altered the staining of nuclei of cells in the hippocampus only 2 weeks after cessation. These results suggest that β-amyloid protein damages the central nervous system in vivo, and that this animal could be used as a model of Alzheimer's disease.

Original languageEnglish
Pages (from-to)411-418
Number of pages8
JournalJapanese Journal of Psychopharmacology
Volume15
Issue number5
Publication statusPublished - 01-01-1995
Externally publishedYes

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Amyloidogenic Proteins
Cerebral Ventricles
Alzheimer Disease
Animal Models
Hippocampus
Choline O-Acetyltransferase
Glial Fibrillary Acidic Protein
Amyloid Plaques
Cell Nucleus
Amyloid
Central Nervous System
Learning
Staining and Labeling
Water

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

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title = "Trial to produce animal model of Alzheimer's disease by continuous infusion of β-amyloid protein into the rat cerebral ventricle",
abstract = "To develop an animal model of Alzheimer's disease, we investigated the toxicity of β-amyloid protein which is a component of senile plaques in Alzheimer's disease. β-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 β-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, β- amyloid protein altered the staining of nuclei of cells in the hippocampus only 2 weeks after cessation. These results suggest that β-amyloid protein damages the central nervous system in vivo, and that this animal could be used as a model of Alzheimer's disease.",
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N2 - To develop an animal model of Alzheimer's disease, we investigated the toxicity of β-amyloid protein which is a component of senile plaques in Alzheimer's disease. β-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 β-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, β- amyloid protein altered the staining of nuclei of cells in the hippocampus only 2 weeks after cessation. These results suggest that β-amyloid protein damages the central nervous system in vivo, and that this animal could be used as a model of Alzheimer's disease.

AB - To develop an animal model of Alzheimer's disease, we investigated the toxicity of β-amyloid protein which is a component of senile plaques in Alzheimer's disease. β-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 β-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, β- amyloid protein altered the staining of nuclei of cells in the hippocampus only 2 weeks after cessation. These results suggest that β-amyloid protein damages the central nervous system in vivo, and that this animal could be used as a model of Alzheimer's disease.

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