Decreased serum and red blood cell kynurenic acid levels in Alzheimer's disease

被引:111
作者
Hartai, Zsuzsanna
Juhasz, Anna
Rimanoczy, Agnes
Janaky, Tamas
Donko, Teodora
Dux, Laszlo
Penke, Botond
Toth, Gabor K.
Janka, Zoltan
Kalman, Janos
机构
[1] Univ Szeged, Albert Szent Gyorgyi Ctr Med & Pharmaceut Sci, Dept Psychiat, H-6725 Szeged, Hungary
[2] Univ Szeged, Dept Med Chem, H-6725 Szeged, Hungary
[3] Univ Szeged, Dept Biochem Med, H-6725 Szeged, Hungary
[4] Univ Szeged, Dept Psychiat, Alzheimers Dis Res Unit, H-6725 Szeged, Hungary
基金
匈牙利科学研究基金会;
关键词
Alzheimer's dementia; kynurenine pathway; kynurenic acid; kynurenine aminotransferase; apolipoprotein E;
D O I
10.1016/j.neuint.2006.08.012
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Kynurenine aminotransferases (KAT I and KAT 11) are responsible for the transamination of kynurenine (KYN) to form kynurenic acid (KYNA), an excitatory amino acid receptor antagonist. Since these members of the kynurenine pathway (KP) are proposed to be involved in the pathogenesis of Alzheimer's dementia (AD), the activities of these enzymes and the levels of these metabolites were measured in the plasma and red blood cells (RBCs) of AD and control subjects together with the inheritance of the apolipoprotein (APOE) epsilon 4 allele. KYNA levels were significantly decreased both in the plasma and in the RBCs in AD, but the levels of KYN and the activities of KAT I and KAT 11 remained unchanged. No association has been found with the possession of the F,4 allele. These findings indicate an altered peripheral KP in AD regardless of the APOE status of the probands. (c) 2006 Published by Elsevier Ltd.
引用
收藏
页码:308 / 313
页数:6
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