The deficiency pattern of neurotransmitters is heterogeneous in patients with Parkinson's disease. Consequence is an individual variable expression of motor and nonmotor features. They respond to agents with a broader spectrum of mode of actions, whereas dopamine substitution only targets impaired motor behavior. The pharmacological profile of safinamide includes reversible monoamine oxidase B inhibition and modulation of voltage-dependent sodium- and calcium channels with consecutive decline of glutamate release. Safinamide improves motor and nonmotor symptoms. Combination of safinamide with the catechol-O-methyltransferase inhibitor opicapone in one capsule is a promising future treatment alternative, which simplifies drug therapy in Parkinson's disease. Both agents complement each other in terms of application mode and efficacy on motor complications as adjuncts to levodopa therapy.
Keywords: Parkinson's disease; glutamate release; levodopa; monoamine oxidase B; opicapone; safinamide.