Pathological Changes of Tau Related to Alzheimer's Disease

被引:58
|
作者
Chu, Dandan [1 ,2 ]
Liu, Fei [3 ]
机构
[1] Nantong Univ, Key Lab Neuroregenerat Jiangsu, Coinnovat Ctr Neuroregenerat, Nantong 226001, Jiangsu, Peoples R China
[2] Nantong Univ, Minist Educ China, Coinnovat Ctr Neuroregenerat, Nantong 226001, Jiangsu, Peoples R China
[3] New York State Inst Basic Res Dev Disabil, Dept Neurochem, Inge Grundke Iqbal Res Floor, Staten Isl, NY 10314 USA
来源
ACS CHEMICAL NEUROSCIENCE | 2019年 / 10卷 / 02期
基金
中国国家自然科学基金;
关键词
tau pathology; Alzheimer's disease; hyperphosphorylation; truncation; aggregation; propagation; PAIRED HELICAL FILAMENTS; REGULATED KINASE 1A; FULL-LENGTH TAU; PROTEIN-TAU; EXON; 10; FRONTOTEMPORAL DEMENTIA; IN-VITRO; ABNORMAL PHOSPHORYLATION; POSTTRANSLATIONAL MODIFICATION; NEUROFIBRILLARY DEGENERATION;
D O I
10.1021/acschemneuro.8b00457
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Alzheimer's disease (AD), the most common form of dementia, is characterized by extracellular beta-amyloid plaques and intracellular neurofibrillary tangles (NFTs), which are considered as major targets for AD therapies. However, no effective therapy is available to cure or prevent the progression of AD up until now. Accumulation of NFTs, which consist of abnormally hyperphosphorylated tau, is directly correlated with the degree of dementia in AD patients. Emerging evidence indicates that the prion-like seeding and spreading of tau pathology may be the key driver of AD. In the past decades, greater understanding of tau pathway reveals new targets for the development of specific therapies. Here, we review the recent research progress in the mechanism underlying tau pathology in AD and briefly introduce tau-based therapeutics.
引用
收藏
页码:931 / 944
页数:27
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