Tau Oligomers: Cytotoxicity, Propagation, and Mitochondrial Damage

被引：236

作者：

Shafiei, Scott S. ^{[1
]}

Guerrero-Munoz, Marcos J. ^{[2
]}

Castillo-Carranza, Diana L. ^{[3
]}

机构：

[1] Univ Texas Med Branch, Dept Neurol Neurosci & Cell Biol, Galveston, TX 77555 USA

[2] Hampton Univ, Dept Chem Engn, Hampton, VA 23668 USA

[3] Hampton Univ, Minor Mens Hlth, Hampton, VA 23668 USA

来源：

FRONTIERS IN AGING NEUROSCIENCE | 2017年 / 9卷

关键词：

tauopathy; tau oligomers; tau secretion; propagation; mitochondrial dysfunction; HEPARAN-SULFATE PROTEOGLYCANS; TRAUMATIC BRAIN-INJURY; V337M HUMAN TAU; ALZHEIMERS-DISEASE; IN-VIVO; NEUROFIBRILLARY TANGLES; EXTRACELLULAR TAU; ENDOGENOUS TAU; MOUSE MODEL; TRANSGENIC MICE;

D O I：

10.3389/fnagi.2017.00083

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

Aging has long been considered as the main risk factor for several neurodegenerative disorders including a large group of diseases known as tauopathies. Even though neurofibrillary tangles (NFTs) have been examined as the main histopathological hallmark, they do not seem to play a role as the toxic entities leading to disease. Recent studies suggest that an intermediate form of tau, prior to NFT formation, the tau oligomer, is the true toxic species. However, the mechanisms by which tau oligomers trigger neurodegeneration remain unknown. This review summarizes recent findings regarding the role of tau oligomers in disease, including release from cells, propagation from affected to unaffected brain regions, uptake into cells, and toxicity via mitochondrial dysfunction. A greater understanding of tauopathies may lead to future advancements in regards to prevention and treatment.

引用

页数：9

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