Peripheral kynurenine metabolism in focal dystonia

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Substantial evidence indicates that neuroactive kynurenine metabolites play a role in the normal physiology of the human-brain, and are involved in the pathology of neurodegenerative disorders such as Parkinson's disease and Huntington's disease. A side-arm product of the pathway, kynurenic acid (KYNA), which is synthesized by the irreversible transamination of kynurenine (KYN) by kynurenine aminotransferases (KAT I and KAT II), is an excitatory amino acid receptor antagonist. In the present study, we measured the level of KYNA and the activities of the biosynthetic enzyme isoforms KAT I and KAT II in the plasma and in the erythrocytes (RBCs) of patients with cervical dystonia or blepharospasm and in age-matched controls. The KAT I and KAT II activities were significantly lower in the plasma of the patients in both subgroups. In the RBCs, only the KAT I activity was elevated significantly. The KYNA concentration was unchanged in both type of patients. These data support the contribution of an altered kynurenine metabolism to the pathogenesis of focal dystonia.

Original languageEnglish
Pages (from-to)285-288
Number of pages4
JournalMedicinal Chemistry
Volume3
Issue number3
DOIs
Publication statusPublished - May 2007

Fingerprint

Kynurenic Acid
Kynurenine
Dystonic Disorders
kynurenine-oxoglutarate transaminase
Blepharospasm
Torticollis
Excitatory Amino Acid Antagonists
Huntington Disease
Glutamate Receptors
Neurodegenerative Diseases
Parkinson Disease
Protein Isoforms
Erythrocytes
Pathology
Brain
Enzymes

Keywords

  • Blepharospasm
  • Cervical dystonia
  • Excitotoxicity
  • Kynurenic acid
  • Kynurenine aminotransferase

ASJC Scopus subject areas

  • Drug Discovery

Cite this

Peripheral kynurenine metabolism in focal dystonia. / Hartai, Zsuzsanna; Klivényi, P.; Janáky, T.; Penke, B.; Dux, L.; Vécsei, L.

In: Medicinal Chemistry, Vol. 3, No. 3, 05.2007, p. 285-288.

Research output: Contribution to journalArticle

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