Metallo-ROS in Alzheimer’s Disease: Oxidation of Neurotransmittersby CuII-b-Amyloid and Neuropathology of the Disease

 

Giordano F. Z. da Silva and Li-June Ming

 

The generation of reactive oxygen species (ROS), including superoxide, peroxide, and free radicals, is associated with normal redox metabolic pathways as side-tracks that can be regulated through the action of superoxide dismutase, catalase, and some reducing agents under homeostasis.[1, 2] However, long-term effects of such oxidative chemical imbalance in normal and disease states can be expected.R OS are often considered the culprits responsible for the devastating effects of oxidative stress,[3] which concern cancer, aging, heart diseases, arthritis, diabetes, and the etiology of neurodegenerative disorders such as Parkinson(s disease and Alzheimer’s disease (AD).[4] AD affects primarily the elderly and causes considerable distress for the patients and emotional suffering of their families and close friends.  One mechanism proposed for the neurodegeneration in AD focuses on amyloid-b peptides (Ab) and their metal complexes through formation of plaques and fibrils and generation of the ROS H2O2 and free radicals.[5–9]

 

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[9] D. A. Butterfield, Curr. Med. Chem. 2003, 10, 2651–2659.

 

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