Journal
NEUROTOXICOLOGY
Volume 80, Issue -, Pages 112-123Publisher
ELSEVIER
DOI: 10.1016/j.neuro.2020.07.003
Keywords
Zinc; Alzheimer's disease; APP; A beta; Tau; BDNF
Categories
Funding
- Hunan Provincial Natural Science Foundation of China [2019JJ50495]
- Scientific Research Fund of Hunan Provincial Education Department [19B476]
- Hengyang Constructive Program [S2018F9031015297]
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Zinc is the second abundant trace element in the human central nervous system (CNS). Zinc homeostasis is impaired in the elderly population and Alzheimer's disease (AD) patients. Due to the failures of beta-amyloid (A beta)- and microtubule-associated protein tau (MAP-tau, tau)-targeting drugs, many researchers consider AD as a multifactorial disease. Emerging evidence demonstrates that zinc is also widely associated with the development of AD. Zinc dyshomeostasis hypothesis of AD has been proposed. In this review, we summarize the role of zinc in A beta production, protein quality control, redox homeostasis, tau phosphorylation, and BDNF signaling. Due to the multifunctional roles of zinc, when zinc dyshomeostasis occurs, it may influence these different biological activities. Zinc dyshomeostasis could be a therapeutic target for AD treatment. However, there is no consensus on the zinc concentration alteration and the effect of zinc overload or zinc deficiency in AD patients, mouse models and cell lines. Given these significant differences across reported studies, it still needs a long time for clinical application in the treatment of AD.
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