| Literature DB >> 29569037 |
Peter Riederer1, Thomas Müller2.
Abstract
This invited narrative review emphasizes the role of MAO-B inhibition in the drug portfolio for dopamine substitution in patients with Parkinson's disease. Neuronal and glial MAO-B inhibition contributes to more stable levels of dopamine and other biogenic amines in the synaptic cleft. Accordingly, symptomatic effects of MAO-B inhibition for a limited amelioration of impaired motor behaviour and wearing-off phenomena in patients with Parkinson's disease are well proven, even when MAO-B inhibitors are only applied together with dopamine agonists. Delay of disease progression by MAO-B inhibition is under debate despite positive experimental findings. This discussion does not consider, that levodopa, respectively, dopamine agonists, are substrates, respectively, inhibitors of the ABCB1 (P-gp, MDR1, and CD243) transporter system. It supports toxin efflux over the blood-brain barrier. ABCB1 transporters have a limited capacity. MAO-B inhibitors do not weaken it. Treatment with MAO-B inhibitors is advantageous as it enables sparing of dopamine agonist and levodopa dosing.Entities:
Keywords: ABCB1 transporter; Monoamine oxidase; Rasagiline; Safinamide; Selegiline
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Year: 2018 PMID: 29569037 DOI: 10.1007/s00702-018-1876-2
Source DB: PubMed Journal: J Neural Transm (Vienna) ISSN: 0300-9564 Impact factor: 3.575