Original Papers

Journal of Neural Transmission

, Volume 64, Issue 2, pp 113-127

First online:

Increased life expectancy resulting from addition of l-deprenyl to Madopar® treatment in Parkinson's disease: A longterm study

  • W. BirkmayerAffiliated withEvangelical Hospital
  • , J. KnollAffiliated withDepartment of Pharmacology, Semmelweis University, Medical School
  • , P. RiedererAffiliated withLudwig Boltzmann-Institute of Clinical Neurobiology, Neurochemistry Group, Lainz-Hospital
  • , M. B. H. YoudimAffiliated withTechnion-Faculty of Medicine, Department of Pharmacology, Rappaport Family Research Institute
  • , Vera HarsAffiliated withDepartment of Clinical Research and Biometrics, Chinoin Pharmaceutical and Chemical Works, Ltd.
  • , J. MartonAffiliated withDepartment of Clinical Research and Biometrics, Chinoin Pharmaceutical and Chemical Works, Ltd.

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In an open, uncontrolled study the longterm (9 years) effect of treatment with Madopar® alone (n=377) or in combination with l-deprenyl (selegiline, selective monoamine oxidase type B inhibitor) (n=564) have been compared in Parkinsonian patients. In patients who lost their response to conventional Madopar therapy the addition of l-deprenyl resulted in a significant recouping of levodopa effect. The survival analysis revealed a significant increase of life expectancy in Madopar-l-deprenyl group regardless of the fact whether or not the significant demographic differences between the two groups were taken into account. Although the mechanism underlying this action of l-deprenyl is not known, the results are interpreted as indicating l-deprenyl's ability to prevent or retard the degeneration of striatal dopaminergic neurons. l-Deprenyl is the first anti-Parkinson drug having such a property. This hypothesis is not far fetched since l-deprenyl selectively prevents the degeneration of striatal dopaminergic neurons induced in animals by the illicit drug l-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Since latter compound is known to cause Parkinsonism in man and primates or Parkinson-like neurochemical and pathological changes in other animals the implications of the present study involving monoamine oxidase activity and l-deprenyl are apparent.