Pentosidine and Nε-(carboxymethyl)-lysine in Alzheimer's disease and vascular dementia

被引:72
作者
Bär, KJ
Franke, S
Wenda, B
Müller, S
Kientsch-Engel, R
Stein, G
Sauer, H
机构
[1] Univ Jena, Dept Psychiat, D-07743 Jena, Germany
[2] Univ Jena, Dept Med, D-07743 Jena, Germany
[3] Univ Jena, Dept Neurol, D-07743 Jena, Germany
[4] Roche Diagnost GmbH, Penzberg, Germany
关键词
advanced glycation end products (AGE); Alzheimer disease; CML; CSF; pentosidine; vascular dementia;
D O I
10.1016/S0197-4580(02)00086-6
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Increasing evidence suggests an interaction of oxidative stress and the formation of advanced glycation end products (AGE) in the onset and progression of Alzheimer's disease. We studied levels of pentosidine and N-epsilon-(carboxymethyl)-lysine (CML) in serum and cerebrospinal fluid (CSF) of 15 patients with probable Alzheimer's disease (AD), 20 patients with vascular dementia (VD), and 31 control subjects (14 matched for age, and 17 younger patients). AGE protein concentrations in CSF did not differ within controls when divided into two subgroups by age. We found significantly elevated levels of CML in CSF of AD patients and of pentosidine in CSF of patients suffering from vascular dementia when compared to controls. The concentrations of pentosidine and CML in serum apparently did not relate directly to CSF values, suggesting influence of extra-cerebral factors in serum samples. It is concluded that AGE proteins are differentially affected in these types of dementia, depending on the specific neuropathology. Furthermore, measurements of AGE products in vivo should rely on CSF rather than blood samples. (C) 2002 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:333 / 338
页数:6
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