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阿尔茨海默病患者血清和红细胞犬尿烯酸水平降低。

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

作者信息

Hartai Zsuzsanna, Juhász Anna, Rimanóczy Agnes, Janáky Tamás, Donkó Teodóra, Dux László, Penke Botond, Tóth Gábor K, Janka Zoltán, Kálmán János

机构信息

Department of Psychiatry, University of Szeged, Szeged, Hungary.

出版信息

Neurochem Int. 2007 Jan;50(2):308-13. doi: 10.1016/j.neuint.2006.08.012. Epub 2006 Oct 4.

Abstract

Kynurenine aminotransferases (KAT I and KAT II) 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) epsilon4 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 II remained unchanged. No association has been found with the possession of the epsilon4 allele. These findings indicate an altered peripheral KP in AD regardless of the APOE status of the probands.

摘要

犬尿氨酸转氨酶(KAT I和KAT II)负责将犬尿氨酸(KYN)转氨生成犬尿喹啉酸(KYNA),后者是一种兴奋性氨基酸受体拮抗剂。由于犬尿氨酸途径(KP)的这些成员被认为参与了阿尔茨海默病性痴呆(AD)的发病机制,因此在AD患者和对照受试者的血浆和红细胞(RBC)中测量了这些酶的活性以及这些代谢产物的水平,并检测了载脂蛋白(APOE)ε4等位基因的遗传情况。AD患者血浆和RBC中的KYNA水平均显著降低,但KYN水平以及KAT I和KAT II的活性保持不变。未发现与ε4等位基因的携带存在关联。这些发现表明,无论先证者的APOE状态如何,AD患者外周的KP均发生了改变。

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