期刊
PHARMACOLOGY
卷 76, 期 1, 页码 19-33出版社
KARGER
DOI: 10.1159/000088929
关键词
Alzheimer; amyloid deposit; oxidative stress; cerebrospinal fluid; protein Tau; neurodegenerative disease
Infusion of Fe2+, A beta(42), and buthionine-sulfoximine (FAB), but not A beta(42) alone or in combination with Fe2+, into the left cerebral ventricle of Long-Evans rats for 4 weeks induced memory impairment that was accompanied by increased hyperphosphorylated Tau protein levels in the CSF. FAB-infused animals displayed thioflavin-S-positive amyloid deposits, hyperphosphorylated Tau protein, neuronal loss, and gliosis. Animals treated with A beta(42), Fe2+, or buthionine- sulfoximine alone or in combination failed to show the histological modifications seen with FAB. This data suggests that A beta(42) is not sufficient to induce an Alzheimer's disease-like symptomatology, and it supports a model whereby a decrease in the brain's antioxidant defense system leads to the A beta(42)-independent oxidative stress necessary for the peptide to induce histopathological changes and memory loss. Copyright (C) 2006 S. Karger AG, Basel.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据