The loss of dopaminergic neurons (DAn) and reduced dopamine (DA) production underlies the reasoning behind the gold standard treatment for Parkinson’s disease (PD) using levodopa (L-DOPA). Recently licensed by the European Medicine Agency (EMA) and US Food and Drug Administration (FDA), safinamide [a monoamine oxidase B (MOA-B) inhibitor] is an alternative to L-DOPA; as we discuss here, it enhances dopaminergic transmission with decreased secondary effects compared with L-DOPA. In addition, nondopaminergic actions (neuroprotective effects) have been reported, with safinamide inhibiting glutamate release and sodium/calcium channels, reducing the excitotoxic input to dopaminergic neuronal death. Effects of safinamide have been correlated with the amelioration of non-motor symptoms (NMS), although these remain under discussion. Overall, safinamide can be considered to have potential antidyskinetic and neuroprotective effects and future trials and/or studies should be performed to provide further evidence for its potential as an anti-PD drug.

多巴胺能神经元（DAn）的丧失和多巴胺（DA）的产生减少是使用左旋多巴（L-DOPA）治疗帕金森氏病（PD）的金标准治疗背后的理由。沙芬酰胺[一种单胺氧化酶B（MOA-B）抑制剂]最近获得了欧洲医学机构（EMA）和美国食品和药物管理局（FDA）的许可，是L-DOPA的替代品；正如我们在这里讨论的，与L-DOPA相比，它增强了多巴胺能传递，而降低了次要作用。另外，已经报道了非多巴胺能作用（神经保护作用），沙非酰胺抑制谷氨酸释放和钠/钙通道，减少了对多巴胺能神经元死亡的兴奋毒性输入。沙芬酰胺的影响与非运动症状（NMS）的改善相关，尽管这些仍在讨论中。全面的，