Cerebral glucose metabolism, cerebrospinal fluid-β-amyloid1-42 (CSF-Aβ42), tau and apolipoprotein E genotype in long-term rivastigmine and tacrine treated Alzheimer disease (AD) patients

被引：40

作者：

Stefanova, E

Blennow, K

Almkvist, O

Hellström-Lindahl, E

Nordberg, A

机构：

[1] Huddinge Univ Hosp, Karolinska Inst, Dept NEUROTEC, Div Mol Neuropharmacol, S-14186 Huddinge, Sweden

[2] Univ Gothenburg, Molndal Hosp, Dept Clin Neurosci, Gothenburg, Sweden

来源：

NEUROSCIENCE LETTERS | 2003年 / 338卷 / 02期

关键词：

Alzheimer's disease; cholinesterase inhibitors; glucose metabolism; positron emission tomography (PET); cerebrospinal fluid-tau (CSF-tau); cerebrospinal fluid-beta-amyloid(1-42) (CSF-A beta 42);

D O I：

10.1016/S0304-3940(02)01384-8

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

We evaluated cerebral glucose metabolism (CMRglc) and cerebrospinal fluid (CSF) levels of tau and beta-amyloid(1-42)(Abeta42), in relation to apolipoprotein E (ApoE) genotype, in patients with mild Alzheimer disease (AD) treated with rivastigmine (n = 11) and tacrine (n = 16) for 1 year; and two untreated AD groups. The rivastigmine-treated AD patients showed a significant increase in CMRglc as compared to both tacrine-treated and untreated AD subjects. The rivastigmine-treated AD group showed no change in CSF-tau levels after 1 year, while in contrast a significant increase as seen in tacrine-treated and untreated AD patients. The CSF-tau changes were mainly seen in ApoE epsilon4 carriers. There was no significant change in Abeta42 after 1-year treatment with either rivastigmine or tacrine. This study shows that the two long-term cholinesterase inhibitor treatments exert different effects on biological markers for AD. (C) 2002 Published by Elsevier Science Ireland Ltd.

引用

页码：159 / 163

页数：5

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