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Titolo:
Kynurenine metabolism in Alzheimer's disease
Autore:
Baran, H; Jellinger, K; Deecke, L;
Indirizzi:
Hosp Psychiat, Ludwig Boltzmann Inst Clin Neurobiol, Vienna, Austria Hosp Psychiat Vienna Austria zmann Inst Clin Neurobiol, Vienna, Austria Univ Vienna, Sch Med, Dept Neurol, Vienna, Austria Univ Vienna Vienna Austria ienna, Sch Med, Dept Neurol, Vienna, Austria
Titolo Testata:
JOURNAL OF NEURAL TRANSMISSION
fascicolo: 2, volume: 106, anno: 1999,
pagine: 165 - 181
SICI:
0300-9564(1999)106:2<165:KMIAD>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
D-ASPARTATE RECEPTOR; LONG-TERM POTENTIATION; ADRDA WORK GROUP; QUINOLINIC ACID; D-CYCLOSERINE; HUMAN-BRAIN; RAT-BRAIN; HUNTINGTONS-DISEASE; AMINOTRANSFERASE-I; CEREBROSPINAL-FLUID;
Keywords:
Alzheimer's disease; kynurenine; kynurenine aminotransferase; kynurenic acid; biosynthesis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
86
Recensione:
Indirizzi per estratti:
Indirizzo: Jellinger, K Ludwigstriazmann Inst Clin Neurobiol, Baumgartner Hohe 1, A-1145 Vienna, Au Ludwig Boltzmann Inst Clin Neurobiol Baumgartner Hohe 1 Vienna Austria A-1145
Citazione:
H. Baran et al., "Kynurenine metabolism in Alzheimer's disease", J NEURAL TR, 106(2), 1999, pp. 165-181

Abstract

L-kynurenine (L-KYN) serves as a substrate for the synthesis of neurotoxic3-OH-kynurenine (3-OH-KYN) and neuroprotective kynurenic acid (KYNA). KYNAis able to interact with ionotropic excitatory amino acid receptors that are involved in a variety of neurodegenerative disorders. The purpose of thepresent study was to investigate the biosynthetic machinery of KYNA in several regions of Alzheimer's disease (AD) brain. The endogenous levels of L-KYN, 3-OH-KYN and KYNA in frontal cortex, caudate nucleus, putamen, hippocampus, and cerebellum of 11 autopsy confirmed cases of AD and 13 age-matchedcontrols were analyzed. Subsequently, the activity of two proteins responsible for the production of KYNA, kynurenine aminotransferases I and II (KATI and KAT II), was investigated. There was a trend for a decrease of L-KYNand 3-OH-KYN in all examined regions of AD brain, as compared to controls. However, KYNA was increased significantly in the putamen and caudate nucleus of AD, by 192 and 177%, respectively. In other areas of AD brain only a minor increase of KYNA was present. Elevated KYNA in the caudate nucleus and putamen correlated with a significant increase of KAT I activities in both nuclei - 157 and 147%, respectively. A minor increase of KAT II was measured only in the caudate nucleus of AD subjects. Kinetic analysis of KAT I and II performed in the caudate nucleus of AD patients revealed a marked increase of V-max, by 207 and 274% of controls, respectively. K-m value for L-KYN using pyruvate as amino acceptor was significantly higher for KAT II (247% of controls). The present data indicate an elevated kynurenine metabolism in AD brain. A marked increase of KYNA in the caudate nucleus and putamen may compensate the hyperactivity of the striato-frontal loop in AD brains. Blockade of NMDA receptors by KYNA may be responsible for impaired memory, learning and cognition in AD patients.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 18:58:31