Influence of beta-amyloid protein and cholesterol on the pathological changes of Alzheimer's disease and expression of nicotinic acetylcholine receptors in rats.
- Author:
Ru-yu LIU
1
;
Ran GU
;
Xiao-lan QI
;
Jia CHEN
;
Jia-liu LIU
;
Zhi-zhong GUAN
Author Information
- Publication Type:Journal Article
- MeSH: Alzheimer Disease; chemically induced; metabolism; pathology; physiopathology; Amyloid beta-Peptides; metabolism; Animals; Cerebral Cortex; metabolism; pathology; Cholesterol; blood; Drug Synergism; Female; Hypercholesterolemia; blood; Learning; drug effects; Male; Peptide Fragments; metabolism; RNA, Messenger; metabolism; Random Allocation; Rats; Rats, Wistar; Receptors, Nicotinic; biosynthesis; genetics
- From: Chinese Journal of Pathology 2007;36(3):184-189
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo 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.
METHODThe 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.
RESULTSAbeta 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.
CONCLUSIONSAbeta can induce marked neuropathological changes, influence the learning and study ability, and modify the expression of nAChRs. Cholesterol can enhance the neurotoxicity of Abeta.
