期刊
NEUROSCIENCE LETTERS
卷 705, 期 -, 页码 183-194出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2019.04.022
关键词
Alzheimer's disease; Tauopathies; Tau; Neurodegeneration; Tau aggregation and propagation; Acetylation; Phosphorylation; Synaptic dysfunction; Glia; Neuroinflammation
资金
- CART Fund
- BrightFocus Foundation [A2016399S]
- Alzheimer's Association [NIRG-15-363678]
- American Federation for Aging Research
- NIH's National Institute for Aging [1R01AG052505]
- National Institute for Neurological Disorders and Stroke [1R01NS095988]
- F31 student fellowship [NS098623]
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.
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