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The Neuroprotective and Neuronal Rescue Effect of (-)-Deprenyl

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Apoptosis and Its Modulation by Drugs

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 142))

Summary

(-)-Deprenyl treatment is able to increase the dopaminergic tone in the CNS by several mechanisms. It inhibits the normal metabolic degradation of dopamine and the metabolites formed from the drug reduce the uptake and promote the release of the transmitter. The age-related increase in MAO-B activity can also be blocked by (-)-deprenyl administration, which can decrease the resulting oxidative damage of the CNS. (-)-Deprenyl pretreatment can inhibit the formation of toxins from pre-toxins and their selective uptake into the nerve endings. In small doses (-)-deprenyl is also effective in post-treatment schedules, having a neuronal rescue effect partly due to the inhibition of apoptosis of the neurones by the drug. (-)-Deprenyl is still the most widely used MAO inhibitor in the treatment of Parkinson’s disease (PD). It is administered alone or in combination with levodopa. The treatment can postpone the need for levodopa or potentiate its effect. The usage of (-)-deprenyl treatment in Alzheimer’s disease (AD) is less frequent than in PD, but some results indicate a mild improvement in cognitive functions of the patients with AD.

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Magyar, K., Szende, B. (2000). The Neuroprotective and Neuronal Rescue Effect of (-)-Deprenyl. In: Cameron, R.G., Feuer, G. (eds) Apoptosis and Its Modulation by Drugs. Handbook of Experimental Pharmacology, vol 142. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-57075-9_18

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