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Emerging approaches in Parkinson’s disease – adjunctive role of safinamide

Authors Müller T

Received 15 May 2016

Accepted for publication 9 July 2016

Published 2 August 2016 Volume 2016:12 Pages 1151—1160


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 4

Editor who approved publication: Professor Garry Walsh

Thomas Müller

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

Abstract: Ongoing neuronal death in Parkinson’s disease (PD) causes an altered neuro­transmission of various biogenic amines, particularly dopamine. As these changes do not follow a distinct pattern, they vary individually, and are differently pronounced. As a result, a heterogeneous onset of motor and nonmotor features occurs in each patient with PD during the whole course of the disease. PD actually describes a set of distinct diseases that manifest themselves in clinical syndromes with certain similarities but also great differences. This clinical picture responds to drugs with a broad spectrum of modes of actions better than to compounds with an exclusive focus on specific receptor subtypes. Therefore, safinamide is an ideal candidate for treatment of patients with PD, since its pharmacological profile includes reversible monoamine oxidase-B inhibition, blockade of voltage-dependent sodium channels, modulation of calcium channels, and inhibition of glutamate release. Safinamide is applied only once daily. Its oral dose ranges from 50 to 100 mg. Safinamide was well tolerated and safe in the clinical development program that demonstrated the amelioration of motor symptoms and OFF phenomena by safinamide when combined with dopamine agonists or levodopa. In the real world of maintenance of patients with PD, effects of safinamide application resemble therapy with classical monoamine oxidase inhibitors or amantadine in combination with other dopamine-substituting drugs. Safinamide is becoming increasingly available in the EU despite complex approval and pricing scenarios.

Keywords: safinamide, MAO-B inhibition, glutamate release inhibition, Parkinson’s disease, dopamine substitution, glutamate

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