Abstract
Alzheimer’s disease (AD) is associated with the abnormal aggregation of amyloid-beta (Aβ) protein. Aβ and its precursor protein (APP) interact with metal ions such as zinc, copper and iron. Evidence shows that these metals play a role in the precipitation and cytotoxicity of Aβ. Despite recent advances in AD research, there is a lack of therapeutic agents to hinder the apparent aggregation and toxicity of Aβ. Recent studies show that drugs with metal chelating properties could produce a significant reversal of amyloid-β plaque deposition in vitro and in vivo. Here we discuss the interaction of Aβ with metals, metal dyshomeostasis in the CNS of patients with AD, and the potential therapeutic effects of metal chelators.
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Cuajungco, M.P., Frederickson, C.J., Bush, A.I. (2005). Amyloid-β Metal Interaction and Metal Chelation. In: Harris, J.R., Fahrenholz, F. (eds) Alzheimer’s Disease. Subcellular Biochemistry, vol 38. Springer, Boston, MA . https://doi.org/10.1007/0-387-23226-5_12
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