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Metal dyshomeostasis is a significant factor in many neurodegenerative diseases, through mechanisms that include oxidative damage via abnormal protein metal chemistry and/or the formation of aggregates or fibrils.
Proteins include amyloid-beta (Ab) in Alzheimer’s disease (AD), Cu–Zn superoxide dismutase (SOD1) in amyotrophic lateral sclerosis (ALS) and prion protein (PrP) in human Creutzfeldt–Jakob disease and bovine spongiform encephalopathy in cattle. There is evidence that binding of copper to amyloid precursor protein (APP) leads to the reduction of Ab production and lowers AD progression.