ABSTRACT

Neurons of the central nervous system are subject to a number of unique conditions that make them particularly vulnerable to oxidative stress and its sequelae that can culminate in cell death [1]. This vulnerability is a likely consequence of the high energy and oxygen consumption rates, the high unsaturated lipid content of the neuronal membrane, the high levels of transition metals, the relative scarcity of antioxidant defense systems as compared to other organs, and the postmitotic nature of neuronal populations [2]. Although there is debate on whether oxidative stress is a cause or a consequence of the disease, evidence showing oxidative stress before any other known change indicates a causative role in the pathogenesis of Alzheimer’s disease (AD).