Genetic analysis of the genome of AD patients revealed that a cohort of single nucleotide polymorphisms in ATP7B account for imbalances in circulating nonceruloplasmin-bound copper which increase the risk of AD, supporting the notion that changes in copper homeostasis may accelerate the neurodegeneration that lead to AD (Bucossi et al., 2011; Bucossi et al., 2013; Squitti et al., 2013). This evidence concerns the gene ATP7B and Alzheimer disease.