Potential Pathways of Abnormal Tau and α-Synuclein Dissemination in Sporadic Alzheimer's and Parkinson's Diseases
Potential Pathways of Abnormal Tau and α-Synuclein Dissemination in Sporadic Alzheimer's and Parkinson's Diseases
复制标题
DOI：
10.1101/cshperspect.a023630
复制
发表时间：
2016-11-01
影响因子：
7.2
通讯作者：
Del Tredici, Kelly
中科院分区：
文献类型：
--
作者：
Braak, Heiko;Del Tredici, Kelly
实验数据表明，在散发性阿尔茨海默病(AD)和帕金森病(PD)等神经退行性蛋白病中，异常蛋白聚集体的跨神经元传播能够自我传播，导致神经退行性变的进展和蛋白样粒子的积累。错误折叠的tau和α-突触核蛋白可能从神经链中的一个神经细胞扩散到下一个神经细胞，导致异常聚集的机制仍不清楚。基于对人类尸检病例的研究结果，我们回顾了tau(散发性AD)和α-突触核蛋白(散发性PD)聚集体在解剖学上相互连接的区域之间轴突和跨神经元扩散的潜在途径和机制。
Experimental data indicate that transneuronal propagation of abnormal protein aggregates in neurodegenerative proteinopathies, such as sporadic Alzheimer's disease (AD) and Parkinson's disease (PD), is capable of a self-propagating process that leads to a progression of neurodegeneration and accumulation of prion-like particles. The mechanisms by which misfolded tau and alpha-synuclein possibly spread from one involved nerve cell to the next in the neuronal chain to induce abnormal aggregation are still unknown. Based on findings from studies of human autopsy cases, we review potential pathways and mechanisms related to axonal and transneuronal dissemination of tau (sporadic AD) and alpha-synuclein (sporadic PD) aggregates between anatomically interconnected regions.