Prion-like propagation of pathology in Parkinson disease.
Prion-like propagation of pathology in Parkinson disease.
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DOI：
10.1016/b978-0-444-63945-5.00017-9
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发表时间：
2018
影响因子：
--
通讯作者：
Brundin P
中科院分区：
文献类型：
--
作者：
Volpicelli-Daley L;Brundin P
100多年前，路易体和路易神经突被定义为帕金森病的病理标志。80年后，α-突触核蛋白被发现是这些包涵体的主要成分。新出现的证据表明，α-突触核蛋白病理学以朊病毒样方式在整个神经系统的互连网络中传播。病理性α-突触核蛋白导致天然α-突触核蛋白聚集，导致形成不溶性包涵体。这些种子可以在神经元内传播并传播到相互连接的神经元，导致病理学在整个大脑中传播。在这里，我们讨论了α-突触核蛋白病理学在整个神经系统中传播的发现如何彻底改变了我们对帕金森病发病机制的理解，并导致了新的治疗策略的发展，以阻止疾病的进展。
Over 100 years ago, Lewy bodies and Lewy neurites were defined as a pathological hallmark of Parkinson’s disease. Eighty years later, α-synuclein was found to be the primary component of these inclusions. Emerging evidence suggests that α-synuclein pathology propagates across interconnected networks throughout the nervous system in a prion-like manner. Pathologic α-synuclein seeds aggregation of native α-synuclein, resulting in the formation of insoluble inclusions. These seeds can propagate within the neuron and to interconnected neurons, resulting in the spread of pathology throughout the brain. Here, we discuss how the findings that α-synuclein pathology spreads throughout the nervous system has revolutionized our understanding about Parkinson’s disease pathogenesis and resulted in the development of novel therapeutic strategies to halt disease progression.