Copper is an indispensable biometal participating as a redox catalyst in many important biochemical processes. However, if uncontrolled, copper ions induce the formation of reactive oxygen species and become toxic. For this reason, cellular copper metabolism is tightly regulated and specific proteins – copper chaperones – participate in the metalation of cellular copper transporters and enzymes. The thermodynamic background for cellular copper distribution is known, and copper is driven to cellular destinations according to shallow affinity gradients. Copper metabolism is disturbed in the case of Wilson’s, Menkes, and Alzheimer’s disease (AD), characterized by copper overload, deficiency, and misdistribution, respectively. Wilson’s and Menkes disease could be treated by copper chelators and supplements, respectively; however, with AD, a search for effective molecular tools for the correction of copper metabolism is ongoing. One natural copperbinding ligand – α-lipoic acid – has shown positive results in cellular and fruit fly models of AD and serves as a promising candidate for the regulation of copper metabolism in the case of AD.
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