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(-)-Deprenyl (D)/Selegiline, introduced under the code name: E-250, in 1964/65 as a new spectrum "psychic energizer" (Knoll et al., 1965), and named (-)-deprenyl from 1970, became famous in 1971/1972 as the first selective inhibitor of B-type monoamine oxidase (MAO-B) (Knoll  Magyar, 1972). D, registered at present in 64 countries, started its world-wide carrier as a therapeutic agent in 1977 as the unique MAO inhibitor free of the cheese-effect (reviewing its early history see Knoll, 1983). In the early 1960s when Knoll developed D MAO inhibitors were at the center of interest. It was the period when the hypothesis that depression is associated with diminished monoaminergic tone in the brain took root in the scientific community. MAO inhibitors played a key role in the development of this hypothesis. It became clear that MAO inhibitors elated depressed patients because they enhance the biological activity of monoamine transmitters in the central nervous system. In 1951 isoniazid and its isopropyl-derivative, iproniazid, were successfully introduced for the treatment of tuberculosis and it was an unexpected observation that in contrast to isoniazid, iproniazid produced undesirable central stimulation in some patients. Zeller, who proposed in 1938 the name “monoamine oxidase” for the class of enzymes responsible for the oxidative deamination of monoamines, discovered in 1952 that iproniazid is capable to inhibit MAO activity in the brain and isoniazid is devoid of this property (Zeller  Barsky, 1952). In 1956 Crane analyzed the psychiatric side effects of iproniazid and concluded that it might be beneficial in the treatment of depression (Crane, 1956) and Kline introduced it as a “psychic energizer” (Kline, 1958). Series of new MAO inhibitors were soon developed. It was, however, observed in 1963 that after eating cheese depressive patients treated with the highly potent MAO inhibitor, tranylcypromine, develop temporary clinical symptoms similar to a paroxysm induced by pheochromocytoma: hypertension, palpitation, neck stiffness, headache, nausea, vomiting. The same was observed also during treatment with nialamid, pargyline, and other MAO inhibitors. Blackwell (1963) realized that the hypertensive crisis is associated with the ingestion of high amounts of tyramine in cheese, the metabolism of which is inhibited by the MAO inhibitors (“cheese-effect”). Similar clinical episodes have also been observed after the ingestion of some other foodstuffs, such as yeast products and chianti wines, pickled herring, chicken liver, which are rich in tyramine, and/or other amine such as -phenylethylamine (PEA), tryptamine, or L-3,4-dihydroxyphenylalanine (L-DOPA).

The Knoll-Concept to Decrease the Prevalence of Parkinson’s Disease