%0 Journal Article
%T Early Onset Alzheimer¡¯s Disease and Oxidative Stress
%A Marco Antonio Meraz-R¨ªos
%A Diana Franco-Bocanegra
%A Danira Toral Rios
%A Victoria Campos-Pe£¿a
%J Oxidative Medicine and Cellular Longevity
%D 2014
%I Hindawi Publishing Corporation
%R 10.1155/2014/375968
%X Alzheimer¡¯s disease (AD) is the most common cause of dementia in elderly adults. It is estimated that 10% of the world¡¯s population aged more than 60¨C65 years could currently be affected by AD, and that in the next 20 years, there could be more than 30 million people affected by this pathology. One of the great challenges in this regard is that AD is not just a scientific problem; it is associated with major psychosocial and ethical dilemmas and has a negative impact on national economies. The neurodegenerative process that occurs in AD involves a specific nervous cell dysfunction, which leads to neuronal death. Mutations in APP, PS1, and PS2 genes are causes for early onset AD. Several animal models have demonstrated that alterations in these proteins are able to induce oxidative damage, which in turn favors the development of AD. This paper provides a review of many, although not all, of the mutations present in patients with familial Alzheimer¡¯s disease and the association between some of these mutations with both oxidative damage and the development of the pathology. 1. Introduction Brain requires a high consumption of oxygen to generate adenosine triphosphate (ATP). It is known that oxygen metabolism in the mitochondria, endoplasmic reticulum (ER), and peroxisomes generates oxidant agents known as free radicals [1, 2], small molecules with unpaired electron that includes the oxygen reactive species (ROS) like hydroxyl radical ( ), superoxide radical ( ), the reactive nitrogen species (RNS), and nitric oxide ( ). These molecules show high reactivity with macromolecules [3] and have an important biological function as signaling molecules [4]. However the interaction of these agents and nonradical oxidants with membrane lipids, proteins, and DNA also could be conducted to cellular senescence. This oxidative damage is catalyzed by the presence of trace elements Fe, Cu or both [5]. As part of evolution, organisms have developed enzymatic and nonenzymatic antioxidants mechanism to counteract oxidative damage, which act removing free radicals, scavenging ROS/RNS or their precursors and binding trace elements [1]. The antioxidant enzymes are superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx). The nonenzymatic antioxidants group is composed of the natural molecules glutathione (GSH) and the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH), and compounds like ascorbic and lipoic acid, polyphenols and carotenoids dietary derived [6]. However, an imbalance of oxidants and antioxidants agents could generate oxidative
%U http://www.hindawi.com/journals/omcl/2014/375968/