Copper and zinc level alterations in the brain structures in Parkinson’s and Alzheimer’s diseases

Abstract

The article reviews the literature on copper and zinc level alterations in the brain structures in neurodegenera-tive diseases (Parkinson's disease, PD, and Alzheimer's disease, AD). We discuss the ability of these micro-elements to bind to cellular proteins (α-synuclein in PD and β-amyloid in AD) disrupting their metabolism. The literature analysis shows that high copper levels in the neurons of nigrostriatal brain formations in PD initiate oxidative stress development. Copper extracellular deficiency disturbs iron metabolism and thus may increase the stress. Low zinc levels weaken the enzyme antioxidant potential. In AD, disruption of the homeostasis of these metals in the brain structures has a different effect. In the early stages, the complex formed by β-amyloid and copper (II) ions is involved in a series of redox reactions, resulting in the formation of free radicals which stimulate the expression of neuroinflammatory mediator, accompanied by uncontrolled release of zinc, high concentrations of which catalyzing the formation of the toxic forms of aggregated Aβ. Keywords: brain, copper, zinc, Parkinson’s disease, Alzheimer’s disease