Abstract
Copper (Cu) is an essential trace metal, and either a Cu deficiency or excess is life-threatening. Recent studies have indicated that an imbalance of Cu levels and a high burden of oxidative stress are contributors of Alzheimer's disease (AD), the main cause of dementia in the elderly. AD Cu imbalance can be described as a reduction of functional Cu bound to proteins and a shift of the metal to the non-ceruloplasmin (non-Cp) Cu pool, prone to oxidative stress. The shift/displacement of the metal from bound to labile toxic Cu in the brain can explain mitochondrial deficits, energy depletion, protein misfolding of amyloid beta, and other proteins associated to dementia. We suggest a diet-gene interplay at the basis of the “CuAD,” a subset of AD patients typified by higher-than-normal non-Cp Cu. A description of the Cu-regulating pathways and suggestions for a low-copper diet to improve preventive strategies are reported herein.
Published Version
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