Tau Filaments and the Development of Positron Emission Tomography Tracers.

Tau Filaments and the Development of Positron Emission Tomography Tracers.
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DOI:
10.3389/fneur.2018.00070
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发表时间:
2018
影响因子:
3.4
通讯作者:
Sahara N
Sahara N
中科院分区:
医学3区
文献类型:
--
作者:
Goedert M;Yamaguchi Y;Mishra SK;Higuchi M;Sahara N

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从可溶性单体到不溶性丝状Tau的病理途径被认为是人类Tau病的基础。额颞叶痴呆的病例是由Tau基因MAPT的显性遗传突变引起的。他们表明Tau蛋白的功能障碍足以导致神经变性和痴呆。外推到更常见的散发性Tau病,人们可以得出这样的结论:病理途径对所有疾病病例的发展至关重要,即使Tau组装有多种原因。这些发现在概念上类似于β-淀粉样蛋白,α-突触核蛋白和朊病毒蛋白的报道。在这里,我们提供了一个概述的Tau丝及其正电子发射断层扫描配体。
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 MAPT, 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.
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影响因子: --
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