Is selegiline neuroprotective in Parkinson’s disease?

  • M. Gerlach
  • M. B. H. Youdim
  • P. Riederer
Part of the Journal of Neural Transmission book series (NEURAL SUPPL, volume 41)


Recent findings emphasize the significance of oxidative mechanisms, involving the activity of monoamine oxidase (MAO) and the formation of free radicals, in the pathogenesis of Parkinson’s disease. The possible role of such mechanisms in the degeneration of neurones in the substantia nigra has led to clinical trials aimed at preventing or slowing the progressively disabling course of the disease. However, conclusive clinical evidence of a neuroprotective effect in PD is still lacking. In this paper, we discuss possible mechanisms by which selegiline manifests neuroprotective effects in experimental and clinical situations. Besides MAO-B inhibition, which above all explains the prevention of protoxin activation and substrate oxidation by MAO-B, selegiline appears to exhibit other mechanisms of action (induction of Superoxide dismutase, stimulation of neurotrophic factor synthesis, antagonistic modulation of the polyamine binding site of the NMDA-receptor) which are independent of its action on MAO-B.


Tyrosine Hydroxylase Neuroprotective Effect Monoamine Oxidase Excitatory Amino Acid Excitatory Amino Acid Receptor 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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Copyright information

© Springer-Verlag 1994

Authors and Affiliations

  • M. Gerlach
    • 1
    • 2
  • M. B. H. Youdim
    • 3
  • P. Riederer
    • 1
  1. 1.Clinical NeurochemistryDepartment of PsychiatryWürzburgFederal Republic of Germany
  2. 2.Clinical Neurochemistry, Department of NeurologyUniversity of Bochum, St. Joseph HospitalBochumFederal Republic of Germany
  3. 3.Department of PharmacologyTechnionHaifaIsrael

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