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Oxidative Medicine and Cellular Longevity
Volume 2014, Article ID 497802, 11 pages
Review Article

Oxidative Stress and Metabolic Syndrome: Cause or Consequence of Alzheimer's Disease?

1Facultad de Ciencias Químicas, Universidad Autónoma de Coahuila, Boulevard V. Carranza S/N, Colonia República Oriente, Saltillo, COAH, Mexico
2Laboratorio de Nutrición Experimental, Instituto Nacional de Pediatría, Insurgentes Sur 3700 letra C, Coyoacán, 04530 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
4Universidad Nacional Autónoma de México, Avenida Insurgentes Sur 3000, Coyoacán, 04510 Mexico City, Mexico
5Laboratorio Experimental de Enfermedades Neurodegenerativas, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Insurgentes Sur 3877, 14269 Mexico City, Mexico

Received 12 September 2013; Revised 2 December 2013; Accepted 18 December 2013; Published 20 January 2014

Academic Editor: José Pedraza-Chaverri

Copyright © 2014 Diana Luque-Contreras 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.


Alzheimer’s disease (AD) is a major neurodegenerative disease affecting the elderly. Clinically, it is characterized by a progressive loss of memory and cognitive function. Neuropathologically, it is characterized by the presence of extracellular -amyloid (A) deposited as neuritic plaques (NP) and neurofibrillary tangles (NFT) made of abnormal and hyperphosphorylated tau protein. These lesions are capable of generating the neuronal damage that leads to cell death and cognitive failure through the generation of reactive oxygen species (ROS). Evidence indicates the critical role of A metabolism in prompting the oxidative stress observed in AD patients. However, it has also been proposed that oxidative damage precedes the onset of clinical and pathological AD symptoms, including amyloid- deposition, neurofibrillary tangle formation, vascular malfunction, metabolic syndrome, and cognitive decline. This paper provides a brief description of the three main proteins associated with the development of the disease (A, tau, and ApoE) and describes their role in the generation of oxidative stress. Finally, we describe the mitochondrial alterations that are generated by A and examine the relationship of vascular damage which is a potential prognostic tool of metabolic syndrome. In addition, new therapeutic approaches targeting ROS sources and metabolic support were reported.