Neurotoxins and Monoamine Oxidase B Inhibitors: Possible Mechanisms for the Neuroprotective Effect of (—)-Deprenyl
The 1-methyl-4-phenyl-l,2,3,6-tetrahydropyridine (MPTP) [1–3] model of Parkinson’s disease, which came to light by the accidental self-administration of this protoxin by a group of American drug addicts, has stimulated an enormous amount of research and speculation into the cause of this disorder and the possible role of endo- or exotoxins in its pathogenesis. The fact that (—)-deprenyl (selegiline), the selective monoamine oxidase (MAO) B inhibitor, both prevents the development of MPTP toxicity [4, 5] and appears to slow degeneration of the nigrostri-atal tract in human idiopathic paralysis agitans has lent support to the idea that analogous toxins may be responsible for Parkinson’s disease (PD). They may well be, although there is no convincing evidence for this conclusion at the present time. However, other explanations for the putative neuroprotective effects of (—)-deprenyl are also possible and will be discussed in this chapter.
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