期刊
AGEING RESEARCH REVIEWS
卷 12, 期 1, 页码 174-181出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.arr.2012.06.002
关键词
Alzheimer's disease; Tau kinases; Amyloid plaques
资金
- Canadian Institutes of Health Research
- NSERC
- Alberta Heritage Foundation for Medical Research Senior Scholar
Since its discovery, the hallmarks of Alzheimer's disease (AD) brain have been recognised as the formation of amyloid plaques and neurofibrillary tangles (NFTs). Mounting evidence has suggested the active interplay between the two pathways. Studies have shown that beta-amyloid (A beta) can be internalized and generated intracellularly, accelerating NFT formation. Conversely, tau elements in NFTs are observed to affect A beta and amyloid plaque formation. Yet the precise mechanisms which link the pathologies of the two brain lesions remain elusive. In this review, we discuss recent evidence that support five putative mechanisms by which crosstalk occurs between amyloid plaque and NFT formation in AD pathogenesis. Understanding the crosstalks in the formation of AD pathologies could provide new clues for the development of novel therapeutic strategies to delay or halt the progression of AD. (c) 2012 Elsevier B.V. All rights reserved.
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