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Zhonghua Bing Li Xue Za Zhi ; 36(3): 184-9, 2007 Mar.
Article in Chinese | MEDLINE | ID: mdl-17535686

ABSTRACT

OBJECTIVE: To study the influence of beta-amyloid protein (Abeta) and cholesterol on the pathological changes of Alzheimer's disease (AD) and on the expression of nicotinic acetylcholine receptor (nAChR) subunits in the brains of rats. METHOD: The rats were treated by intracerebroventricular injection of Abeta1-42 and fed with a diet containing 5% cholesterol to establish animal model of AD. The pathological changes, learning and memory, and expression of nAChRs of rats were analyzed by Bieoschowsky staining, immunohistochemistry, water-labyrinth, Western blot, and RT-PCR. RESULTS: Abeta intracerebroventricular injection induced Abeta deposition in rat brains and high-cholesterol diet resulted in hypercholesterolemia in the animals. Injection of Abeta caused a reduction of learning and memory of rats and modifications of the expression of nAChRs. Cholesterol enhanced these effects of Abeta on neuropathology and expression of nAChRs. CONCLUSIONS: Abeta can induce marked neuropathological changes, influence the learning and study ability, and modify the expression of nAChRs. Cholesterol can enhance the neurotoxicity of Abeta.


Subject(s)
Alzheimer Disease/pathology , Cerebral Cortex/pathology , Learning/drug effects , Receptors, Nicotinic/biosynthesis , Alzheimer Disease/chemically induced , Alzheimer Disease/metabolism , Alzheimer Disease/physiopathology , Amyloid beta-Peptides/metabolism , Animals , Cerebral Cortex/metabolism , Cholesterol/blood , Drug Synergism , Female , Hypercholesterolemia/blood , Male , Peptide Fragments/metabolism , RNA, Messenger/metabolism , Random Allocation , Rats , Rats, Wistar , Receptors, Nicotinic/genetics
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