Journal
AGEING RESEARCH REVIEWS
Volume 35, Issue -, Pages 265-290Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.arr.2016.10.003
Keywords
Metal ions; Oxidative stress; Synaptic plasticity; Neurotoxicity; Autophagy; Apoptosis; Cognitive decline; Alzheimer's disease
Categories
Funding
- National Natural Science Foundation of China [31571064, 81500934, 31300777, 31371091]
- Fundamental Research Funds of China [N152004004, N142004002, N130120002, N120520001, N120320001, N141008001/7, L1520001]
- National Natural Science Foundation of Liaoning, China [2015020662]
- Liaoning Provincial Talent Support Program [LJQ2013029]
- Lvgu Research Foundation
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Alzheimer's disease (AD) is a common form of dementia in aged people, which is defined by two pathological characteristics: beta-amyloid protein (A beta) deposition and tau hyperphosphorylation. Although the mechanisms of AD development are still being debated, a series of evidence supports the idea that metals, such as copper, iron, zinc, magnesium and aluminium, are involved in the pathogenesis of the disease. In particular, the processes of A beta deposition in senile plaques (SP) and the inclusion of phosphorylated tau in neurofibrillary tangles (NFTs) are markedly influenced by alterations in the homeostasis of the aforementioned metal ions. Moreover, the mechanisms of oxidative stress, synaptic plasticity, neurotoxicity, autophagy and apoptosis mediate the effects of metal ions-induced the aggregation state of A beta and phosphorylated tau on AD development. More importantly, imbalance of these mechanisms finally caused cognitive decline in different experiment models. Collectively, reconstructing the signaling network that regulates AD progression by metal ions may provide novel insights for developing chelators specific for metal ions to combat AD. (C) 2016 Elsevier B.V. All rights reserved.
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