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The resurgence of neurotransmitter modulation in Parkinson’s disease with safinamide

Authors Müller T

Received 7 January 2015

Accepted for publication 12 February 2015

Published 26 March 2015 Volume 2015:5 Pages 11—17

DOI https://doi.org/10.2147/JPRLS.S64896

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Dr Abdul Qayyum Rana


Thomas Müller

Department of Neurology, St Joseph Hospital Berlin-Weißensee, Berlin, Germany

Abstract: The main feature of Parkinson’s disease is slowly ongoing neuronal death. Changes of neurotransmission of biogenic amines, such as dopamine, cause the heterogeneity of motor and non-motor symptoms. Therefore, compounds with a broad spectrum of mechanisms of action are ideal candidates for the treatment of the disease. Safinamide reduces dopamine turnover by reversible monoamine oxidase B inhibition, blockage of voltage-dependent sodium channels, and modulation of calcium channels and of glutamate release. Safinamide requires one-time daily intake within a dose range of 50 and 100 mg. Clinical trials demonstrated that safinamide is well tolerated and safe and ameliorates motor behavior when combined with dopamine agonist only or dopamine agonist and levodopa. Safinamide is a putative, important drug for the therapy of Parkinson’s disease with an efficacy superior to available irreversible monoamine oxidase B inhibitors or N-methyl-D-aspartate receptor antagonists.

Keywords: MAO-B inhibition, glutamate release inhibition, dopamine substitution, glutamate

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