TY - JOUR
T1 - β-Amyloid protein-induced Alzheimer's disease animal model
AU - Nitta, Atsumi
AU - Itoh, Akio
AU - Hasegawa, Takaaki
AU - Nabeshima, Toshitaka
N1 - Funding Information:
This study was supporteind part by grants from the Ministry of Education, Science and Culture (No. 05454148)M, inistry of Health and Welfare Foundation for GeorontologicaSl cienceR esearch( 91A-2406)S, RF Grant for Biomedical Research and Japan Research Foundationf or Clinical Pharmacology.
PY - 1994/3/28
Y1 - 1994/3/28
N2 - To investigate the toxicity of β-amyloid protein which consisted of senile plaques of Alzheimer's disease (AD), this was infused into cerebral ventricle for 14 days by using mini-osmotic pump. The performance of the water maze task in β-amyloid protein-treated rats was impaired. Choline acetyltransferase activity significantly decreased in the frontal cortex and hippocampus. These results suggest that the deposition of β-amyloid protein in the brain is related to the impairment of learning and cholinergic neuronal degeneration, and that β-amyloid protein-treated rats could be used as an animal model for AD.
AB - To investigate the toxicity of β-amyloid protein which consisted of senile plaques of Alzheimer's disease (AD), this was infused into cerebral ventricle for 14 days by using mini-osmotic pump. The performance of the water maze task in β-amyloid protein-treated rats was impaired. Choline acetyltransferase activity significantly decreased in the frontal cortex and hippocampus. These results suggest that the deposition of β-amyloid protein in the brain is related to the impairment of learning and cholinergic neuronal degeneration, and that β-amyloid protein-treated rats could be used as an animal model for AD.
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U2 - 10.1016/0304-3940(94)90239-9
DO - 10.1016/0304-3940(94)90239-9
M3 - Article
C2 - 8086012
AN - SCOPUS:0028177692
SN - 0304-3940
VL - 170
SP - 63
EP - 66
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 1
ER -