DEPRENYL - PHARMACOLOGICAL ASPECTS OF ITS CLINICAL EFFECTS

A review of the properties of (-)-deprenyl indicates that its freedom from potentiation of the pressor effects of tyramine (the ''cheese effect'') cannot be explained solely by a sparing of intestinal MAO activity. Inhibition of intraneuronal or liver MAO-A (or liver microsomal enzymes) is important for the cheese effect associated with non-selective MAO inhibitors. MAO-inhibiting properties of (-)-deprenyl account satisfactorily for its useful role as an adjunct to 1-dopa therapy in Parkinson's disease. It is also possible to explain the controversial beneficial effect of (-)-deprenyl on the progression of Parkinson's disease in terms of MAO inhibition. To be able to determine whether (-)-deprenyl treatment delays the progression of Parkinson's disease, neuronal degeneration of the nigrostriatal dopamine system will have to be tracked in patients receiving the drug. Data are presented that PET or SPECT imaging of the dopamine uptake carrier, using radio-labelled versions of cocaine analogues, may be a suitable tool for assessing the progression of Parkinson's disease.