Table of Contents Author Guidelines Submit a Manuscript
Oxidative Medicine and Cellular Longevity
Volume 2014 (2014), Article ID 375968, 14 pages
http://dx.doi.org/10.1155/2014/375968
Review Article

Early Onset Alzheimer’s Disease and Oxidative Stress

1Departamento de Biomedicina Molecular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Instituto Politécnico Nacional 2508, 07360 Mexico City, Mexico
2Posgrado en Ciencias Biológicas, Universidad Nacional Autónoma de México, Universidad 3000, Coyoacan, 04510 Mexico City, Mexico
3Departamento de Fisiología Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Instituto Politécnico Nacional 2508, 07360 Mexico City, Mexico
4Laboratorio Experimental de Enfermedades Neurodegenerativas, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Insurgentes Sur 3877, 14269 Mexico City, Mexico

Received 12 September 2013; Accepted 18 November 2013; Published 14 January 2014

Academic Editor: Verónica Pérez de la Cruz

Copyright © 2014 Marco Antonio Meraz-Ríos et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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 60–65 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.