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Neurobiochemie und Wirkmechanismus von Selegilin

  • M. Gerlach
  • P. Riederer

Zusammenfassung

Da Selegilin bisher der einzige für die Parkinson-Therapie zugelassene MAO-B-Hemmstoff ist, wird im folgenden Absatz vorwiegend nur auf die Mechanismen eingegangen, die dessen klinischen Effekt erklären können. Dieser Wirkstoff wurde ursprünglich nur deshalb für eine Erprobung in der Parkinson-Therapie ausgewählt, weil er in verschiedenen experimentellen pharmakologischen Versuchsmodellen nur eine geringe Verstärkung der sympathikomimetischen Wirkung von Tyramin zeigte (zur übersicht: Finberg und Tenne 1982) und deshalb eine geringe Wahrscheinlichkeit für das Auftreten des „Cheese Effektes“ zu erwarten war. Später wurde erkannt, daß die regionale und zelluläre Verteilung der MAO im Gehirn, das Verhältnis beider Isoformen im Gehirn, die Substrat-Spezifität und die Hemmstoff-Sensitivität unterschiedlich sind zwischen der Ratte (dem Tier, mit dem fast alle präklinischen Untersuchungen durchgeführt wurden) und dem Menschen (Squires 1972, Youdim et al.

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© Springer-Verlag Wien 1999

Authors and Affiliations

  • M. Gerlach
  • P. Riederer

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