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Catechol-O-methyl transferase

About: Catechol-O-methyl transferase is a research topic. Over the lifetime, 1646 publications have been published within this topic receiving 87360 citations.


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Journal ArticleDOI
TL;DR: Overall, there is no significant association of PD with the DAT1‐3′–variable numbers of tandem repeats, the MAO‐B‐(GT)n, and the COMT‐Val108Met gene polymorphisms in a sample of 319 unrelated PD cases and 196 control subjects.
Abstract: We investigated the association of Parkinson's disease (PD) with dopamine transporter-1 (DAT1), monoamine oxidase-B (MAO-B), and catechol-O-methyltransferase (COMT) gene polymorphisms. Overall, we observed no significant association of PD with the DAT1-3'-variable numbers of tandem repeats, the MAO-B-(GT)(n), and the COMT-Val108Met gene polymorphisms in a sample of 319 unrelated PD cases and 196 control subjects. Analyses stratified by sex, age at examination, family history of PD, and ethnic origin also yielded negative findings, with three exceptions. We found statistically significant associations of PD with MAO-B polymorphisms in older patients and with a COMT polymorphism in younger subjects and in women. These significant differences at the two-tailed alpha level of 0.05 and restricted to subgroup analyses may have a biological basis or may be chance findings.

47 citations

Journal ArticleDOI
TL;DR: The results support previous reports of a COMT-genotype-dependent difference in amygdala responsivity as well as connectivity, and highlight the importance of naturally occurring genetic variations in the catecholaminergic system for neural activity underlying affective processing.

47 citations

Journal Article
TL;DR: A possible beneficial effect of OR-462 in the therapy of Parkinson's disease is suggested after a dose-related and long-lasting increase in striatal L-dopa and dopamine levels as well as a reduction in 3-O-methyldopa levels were shown.
Abstract: A selective catechol-O-methyltransferase inhibitor, OR-462, was studied for its ability to affect pharmacokinetic properties of L-dopa after the p.o. administration of the inhibitor to rats and mice. When OR-462 was given to rats at the dose range of 0.3 to 30 mg/kg in conjunction with L-dopa and carbidopa, a dose-related and long-lasting (greater than 5 hr) increase in striatal L-dopa and dopamine levels as well as a reduction in 3-O-methyldopa levels were shown. For a 50% reduction of the 3-O-methyldopa levels a dose of 6 mg/kg of OR-462 was needed. The increase in striatal homovanillic acid, an O-methylated metabolite of dopamine which poorly penetrates the blood brain barrier, indicates that O-methylation was not inhibited in the brain. In order to get the same dopamine levels in striatum the L-dopa dose could be lowered to one-fourth when OR-462 was added. The L-dopa-sparing effect of OR-462 given p.o. was also demonstrated in two behavioral parkinsonian models. OR-462 given at doses of 3 to 30 mg/kg in conjunction with L-dopa and carbidopa, dose-dependently potentiated the L-dopa-induced reversal of hypoactivity in reserpinized mice. Likewise, the same doses of OR-462 caused a marked potentiation of L-dopa-induced contralateral turning behavior in rats with unilateral nigrostriatal lesions produced by 6-hydroxydopamine. The data suggest a possible beneficial effect of OR-462 in the therapy of Parkinson's disease.

46 citations

Journal ArticleDOI
TL;DR: Results do not support the hypothesis that the catechol- O -methyl transferase (COMT) Val 158 Met or BDNF C 270 T gene polymorphisms are associated with liability to schizophrenia.

46 citations

Journal ArticleDOI
TL;DR: The results do not support a direct effect of COMT val158met genotype on performance on neuropsychological measures of attention and executive function, but they suggest that genotype may interact with dopaminergic medication use to influence cognitive ability.
Abstract: Cognitive dysfunction is one of the most incapacitating non-motor symptoms of Parkinson's disease (PD). Some cognitive deficits are thought to be related to abnormal dopamine homeostasis. The latter is influenced by catechol-O-methyltransferase (COMT), an enzyme that degrades dopamine. Previous research suggests a relationship between the COMT val158met functional polymorphism (SNP) and measures of executive function. We evaluated this hypothesis in a cohort of PD patients with an extensive neuropsychological test battery. Cognitive assessment and COMT genotyping were performed in 153 early PD patients from outpatient clinics general hospitals in the Netherlands. Our results do not support a direct effect of COMT val158met genotype on performance on neuropsychological measures of attention and executive function, but they suggest that genotype may interact with dopaminergic medication use to influence cognitive ability.

46 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202338
202265
202129
202032
201931
201834