Unitat de Neuroimmunologia Clínica, Centre d'Esclerosi Múltiple de Catalunya (CEM-Cat), Vall d'Hebron Institut de Recerca(VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
Clin Immunol. 2012 Jan;142(1):84-92. doi: 10.1016/j.clim.2011.06.004. Epub 2011 Jun 25.
Multiple sclerosis (MS) is a neurodegenerative disease that is deemed to affect more than 2.1 million people worldwide, and for which there is no cure. Early symptoms of MS are believed to result from axonal demyelination leading to slowing or blockade of impulse conduction. The blockade of K+ channels has been proven to improve conduction deficiencies secondary to demyelination in patients with MS. Dalfampridine is a K+ channel blocker that was recently approved by FDA for the symptomatic treatment of ambulation hardship in MS. Understanding the mechanisms by which Dalfampridine exerts its therapeutic effects is a complex issue as it blocks a wide variety of K+ channels that are distributed across multiple cell types in the nervous system but also in the immune system, and because of their molecular identities remaining unknown. This review describes Dalfampridine potential roles at the cellular and molecular levels in MS pathogenesis.
多发性硬化症(MS)是一种神经退行性疾病,据认为全球有超过 210 万人受其影响,而且目前尚无治愈方法。MS 的早期症状被认为是轴突脱髓鞘导致冲动传导减慢或阻滞所致。现已证实,钾通道阻断可改善 MS 患者脱髓鞘引起的传导缺陷。地夫可特是一种钾通道阻断剂,最近被 FDA 批准用于治疗 MS 的运动障碍症状。了解地夫可特发挥治疗作用的机制是一个复杂的问题,因为它阻断了分布在神经系统和免疫系统的多种细胞类型中的多种钾通道,而且由于其分子身份仍然未知。这篇综述描述了地夫可特在 MS 发病机制中的细胞和分子水平上的潜在作用。