Journal
ACS CHEMICAL NEUROSCIENCE
Volume 10, Issue 2, Pages 931-944Publisher
AMER CHEMICAL SOC
DOI: 10.1021/acschemneuro.8b00457
Keywords
tau pathology; Alzheimer's disease; hyperphosphorylation; truncation; aggregation; propagation
Funding
- Nantong University, New York State Office for People with Developmental Disabilities
- Neural Regeneration Co innovation Center of Jiangsu Province
- National Natural Science Foundation of China [81300978]
- U.S. Alzheimer's Association [DSAD-15-363172]
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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.
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