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Jaime Kulisevsky; European Neurological Review, 2016;11(2):101-5 DOI: https://doi.org/10.17925/ENR.2016.11.02.101
Published recently in European Neurological Review the peer-reviewed journal from touchNEUROLOGY, Jaime Kulisevsky discusses the mechanism of action of safinamide in Parkinson's disease (PD). Dopaminergic replacement therapies are prescribed widely to improve motor problems in PD. However, as the disease progresses, the response to levodopa (l-dopa) doses becomes shorter and patients experience symptom recurrence at the end of the dose effect. These so-called OFF periods may become refractory to treatment, and may become associated with disabling motor fluctuations or dyskinesias. In addition to dopamine, glutamate excitotoxicity, resulting from disturbance of the homeostatic balance of neurotransmitters and elevated extracellular levels of glutamate, is potentially an important therapeutic target. Safinamide has been investigated in phase III clinical trials as adjunct therapy to l-dopa in mid- to late-stage fluctuating PD. Adding safinamide to l-dopa increases the time patients' symptoms are controlled - so-called ON time, without increasing troublesome dyskinesia. Although safinamide has dopaminergic actions, recent data have suggested that the long-term effects of safinamide on dyskinesia are related to safinamide state- and use-dependent inhibition of sodium channels and stimulated glutamate release, rather than reduced dopaminergic stimulation. Safinamide's unique dual mechanism of action makes it a valuable treatment option for fluctuating PD patients.
The full peer-reviewed, open-access article is available here:
Disclosure: Jaime Kulisevsky has received honoraria for lecturing or advisory boards from UCB, Zambon, Lundbeck and Abbvie, and research support from Instituto de Salud Carlos III, Spain. This study involves a review of the literature and did not involve any studies with human or animal subjects performed by any of the authors.
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