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Zusammenfassung

Die pathogenetische Bedeutung des striatalen Dopaminmangels bei der ParkinsonKrankheit fand nicht zuletzt durch die Erfolge der L-Dopa-Therapie eine Bestätigung Neben der Substitution von Dopamin wurde versucht, auch durch Eingriffe an anderen Stellen der dopaminergen Transmission zu positiven therapeutischen Effekten zu kommen. Eine Möglichkeit bot die Verzögerung des Dopaminkatabolismus durch Gabe von MAO-Hemmern. Wegen überschießender noradrenerger Aktivität und Auftreten des Cheese-Effekts nach Genuß von Tyramin-haltigen Nahrungsmitteln wurde dieser Weg jedoch zunächst wieder verlassen. Nach Differenzierung von zwei verschiedenen MAO-Typen (Typ A und B), die auch selektiv gehemmt werden können (Johnston 1968), fand das Therapieprinzip erneute Beachtung. Selegilin (L-Deprenyl, Phenylisopropyl-methylpropinylamin HCL) zeigte eine selektive Inhibition der MAOTyp B (Knoll et al. 1967, 1972) und somit keinen Cheese-Effekt. Birkmayer et al. (1975) fanden bei kombinierter Anwendung von L-Dopa und Selegilin eine Potenzierung des antiakinetischen L-Dopa-Effektes und eine Besserung von Fluktuationen.

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Copyright information

© Springer-Verlag Wien 1999

Authors and Affiliations

  • P.-A. Fischer
  • H. Baas

There are no affiliations available

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