The complexity of tau in Alzheimer's disease

被引：254
作者：
Naseri, Nima N. [1 ]
Wang, Hong [2 ]
Guo, Jennifer [3 ]
Sharma, Manu [1 ]
Luo, Wenjie [1 ]
机构：
[1] Weill Cornell Med, Brain & Mind Res Inst, Helen & Robert Appel Alzheimers Dis Res Inst, New York, NY 10065 USA
[2] Eli Lilly & Co, Lilly Corp Ctr, Indianapolis, IN 46285 USA
[3] Univ N Carolina, Chapel Hill, NC 27515 USA
来源：
NEUROSCIENCE LETTERS | 2019年 / 705卷
关键词：
Alzheimer's disease; Tauopathies; Tau; Neurodegeneration; Tau aggregation and propagation; Acetylation; Phosphorylation; Synaptic dysfunction; Glia; Neuroinflammation; PAIRED HELICAL FILAMENTS; HEPARAN-SULFATE PROTEOGLYCANS; MILD COGNITIVE IMPAIRMENT; NEUROFIBRILLARY TANGLES; MOUSE MODEL; PROTEIN-TAU; CEREBROSPINAL-FLUID; PHOSPHORYLATED TAU; MICROGLIAL ACTIVATION; TRANSGENIC MICE;
D O I：
10.1016/j.neulet.2019.04.022
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Alzheimer's disease (AD) is characterized by two major pathological lesions in the brain, amyloid plaques and neurofibrillary tangles (NFTs) composed mainly of amyloid-beta (A beta) peptides and hyperphosphorylated tau, respectively. Although accumulation of toxic AD species in the brain has been proposed as one of the important early events in AD, continued lack of success of clinical trials based on A beta-targetingdrugs has triggered the field to seek out alternative disease mechanisms and related therapeutic strategies. One of the new approaches is to uncover novel roles of pathological tau during disease progression. This review will primarily focus on recent advances in understanding the contributions of tau to AD.
引用
收藏
页码：183 / 194
页数：12
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