Copper and Oxidative Stress in the Pathogenesis of Alzheimer’s Disease

• Published in: Biochemistry (Easton) Vol. 51; no. 32; pp. 6289 - 6311
• Main Authors: Eskici, Gözde, Axelsen, Paul H
• Format: Journal Article
• Language: English
• Published: United States American Chemical Society 14.08.2012
• Subjects: Alzheimer disease; Alzheimer Disease - drug therapy; Alzheimer Disease - etiology; Alzheimer Disease - metabolism; Amyloid beta-Peptides - metabolism; Amyloid beta-Protein Precursor - metabolism; binding sites; Biological Transport; brain; Chelating Agents - therapeutic use; copper; Copper - metabolism; Humans; oxidation; Oxidative Stress; pathogenesis; transporters; zinc
• ISSN: 0006-2960; 1520-4995; 1520-4995
• DOI: 10.1021/bi3006169

Copper is a redox-active metal with many important biological roles. Consequently, its distribution and oxidation state are subject to stringent regulation. A large body of clinicopathological, circumstantial, and epidemiological evidence suggests that the dysregulation of copper is intimately involved in the pathogenesis of Alzheimer’s disease. Other light transition metals such as iron and zinc may affect copper regulation by competing for copper binding sites and transporters. Therapeutic interventions targeting the regulation of copper are promising, but large gaps in our understanding of copper biochemistry, amyloidogenesis, and the nature of oxidative stress in the brain must be addressed.