Department of Neurology, Hospital Universitario Reina Sofía, 14004 Cordoba, Spain; University Bordeaux, CNRS, IMN, UMR 5293, 33000 Bordeaux, France.
University Bordeaux, CNRS, IMN, UMR 5293, 33000 Bordeaux, France; CHU Bordeaux, Service de Neurologie des Maladies Neurodégénératives, IMNc, 33000 Bordeaux, France; Department of Medicine, University of Otago, Christchurch, and New Zealand Brain Research Institute, Christchurch, New Zealand.
Rev Neurol (Paris). 2022 May;178(5):460-471. doi: 10.1016/j.neurol.2022.03.010. Epub 2022 May 11.
The two commonest groups of neurodegenerative disorders causing movement disorders are synucleinopathies and tauopathies. These disorders are characterised by the accumulation of abnormally misfolded forms of α-synuclein and tau proteins. Our current understanding of their pathogenesis suggests that extracellular forms of these proteins are of major relevance to the mechanism of pathology propagation throughout the brain and disease progression. The most novel approaches to find disease-modifying therapies aim to reduce or block these forms of tau and α-synuclein. This article reviews therapeutic strategies targeting α-synuclein and tau protein which have entered clinical development.
导致运动障碍的两种最常见的神经退行性疾病是突触核蛋白病和神经纤维缠结病。这些疾病的特征是异常错误折叠的α-突触核蛋白和tau 蛋白的积累。我们目前对其发病机制的理解表明，这些蛋白质的细胞外形式与大脑中病理传播和疾病进展的机制密切相关。发现能够改变疾病进程的治疗方法的最新方法旨在减少或阻断这些tau 和α-突触核蛋白的形式。本文综述了已进入临床开发阶段的针对tau 蛋白和α-突触核蛋白的治疗策略。
