Goedert Michel, Yamaguchi Yoshiki, Mishra Sushil K, Higuchi Makoto, Sahara Naruhiko
MRC Laboratory of Molecular Biology, Cambridge, United Kingdom.
RIKEN Global Research Cluster, Wako, Japan.
Front Neurol. 2018 Feb 15;9:70. doi: 10.3389/fneur.2018.00070. eCollection 2018.
A pathological pathway leading from soluble, monomeric to insoluble, filamentous Tau, is believed to underlie human Tauopathies. Cases of frontotemporal dementia are caused by dominantly inherited mutations in , the Tau gene. They show that dysfunction of Tau protein is sufficient to cause neurodegeneration and dementia. Extrapolation to the more common sporadic Tauopathies leads one to conclude that the pathological pathway is central to the development of all cases of disease, even if there are multiple reasons for Tau assembly. These findings are conceptually similar to those reported for beta-amyloid, alpha-synuclein and prion protein. Here, we provide an overview of Tau filaments and their positron emission tomography ligands.
从可溶性单体Tau转变为不溶性丝状Tau的病理途径被认为是人类Tau蛋白病的基础。额颞叶痴呆病例是由Tau基因的显性遗传突变引起的。这些病例表明，Tau蛋白功能障碍足以导致神经退行性变和痴呆。由此推断，对于更常见的散发性Tau蛋白病，即使Tau聚集存在多种原因，该病理途径对于所有病例的发病也至关重要。这些发现与针对β-淀粉样蛋白、α-突触核蛋白和朊病毒蛋白所报道的结果在概念上相似。在此，我们概述了Tau细丝及其正电子发射断层扫描配体。
