Pharmacological treatment and the prospect of pharmacogenetics in Parkinson’s disease
Identifieur interne : 000191 ( Main/Exploration ); précédent : 000190; suivant : 000192Pharmacological treatment and the prospect of pharmacogenetics in Parkinson’s disease
Auteurs : K. Kalinderi [Grèce] ; L. Fidani [Grèce] ; Z. Katsarou [Grèce] ; S. Bostantjopoulou [Grèce]Source :
- International Journal of Clinical Practice [ 1368-5031 ] ; 2011-12.
Abstract
Parkinson disease (PD) is a progressive movement disorder marked by tremor, rigidity, bradykinesia and postural instability. Levodopa (l‐dopa), usually combined with a peripheral dopa decarboxylase inhibitor, has been proved to provide the best symptomatic benefit for PD. However, its long‐term efficacy is limited because of motor complications and drug‐induced dyskinesia. Dopamine agonists, catechol‐O‐methyltransferase inhibitors and monoamine oxidase‐B inhibitors are anti‐parkinsonian (anti‐PD) drugs that have been found to further improve the potency of l‐dopa and prevent the onset of motor complications. However, as PD is a progressive disorder, all the drugs used for its therapy, manifest reduced efficacy and adverse effects with time. Research on the field of pharmacogenetics has pointed out that the genetic variability of each individual determines to a large extent the inter‐individual variability in response to anti‐PD drugs. Clinicogenetic trials show that drug efficacy or toxicity or susceptibility to side effects are features governed by genetic principles. This article is a review of the present pharmacological treatment of PD and current pharmacogenetic data for PD.
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DOI: 10.1111/j.1742-1241.2011.02793.x
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Kalinderi</name><affiliation wicri:level="1"><country xml:lang="fr">Grèce</country><wicri:regionArea>Department of General Biology, Medical School, Aristotle University of Thessaloniki, Thessaloniki</wicri:regionArea><wicri:noRegion>Thessaloniki</wicri:noRegion></affiliation></author><author><name sortKey="Fidani, L" sort="Fidani, L" uniqKey="Fidani L" first="L." last="Fidani">L. Fidani</name><affiliation wicri:level="1"><country xml:lang="fr">Grèce</country><wicri:regionArea>Department of General Biology, Medical School, Aristotle University of Thessaloniki, Thessaloniki</wicri:regionArea><wicri:noRegion>Thessaloniki</wicri:noRegion></affiliation></author><author><name sortKey="Katsarou, Z" sort="Katsarou, Z" uniqKey="Katsarou Z" first="Z." last="Katsarou">Z. 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Levodopa (l‐dopa), usually combined with a peripheral dopa decarboxylase inhibitor, has been proved to provide the best symptomatic benefit for PD. However, its long‐term efficacy is limited because of motor complications and drug‐induced dyskinesia. Dopamine agonists, catechol‐O‐methyltransferase inhibitors and monoamine oxidase‐B inhibitors are anti‐parkinsonian (anti‐PD) drugs that have been found to further improve the potency of l‐dopa and prevent the onset of motor complications. However, as PD is a progressive disorder, all the drugs used for its therapy, manifest reduced efficacy and adverse effects with time. Research on the field of pharmacogenetics has pointed out that the genetic variability of each individual determines to a large extent the inter‐individual variability in response to anti‐PD drugs. Clinicogenetic trials show that drug efficacy or toxicity or susceptibility to side effects are features governed by genetic principles. 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