%0 Journal Article
%T Oxidative Stress and Metabolic Syndrome: Cause or Consequence of Alzheimer's Disease?
%A Diana Luque-Contreras
%A Karla Carvajal
%A Danira Toral-Rios
%A Diana Franco-Bocanegra
%A Victoria Campos-Pe£¿a
%J Oxidative Medicine and Cellular Longevity
%D 2014
%I Hindawi Publishing Corporation
%R 10.1155/2014/497802
%X 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. 1. Introduction It has been speculated that the free radicals produced during oxidative stress are pathologically important in AD and other neurodegenerative diseases. Oxidative stress can be defined as an imbalance between ROS production and/or their elimination. That oxidative stress implicated in the etiology of AD is possibly due to changes in the redox status that occur in AD brains [1]. In recent years, it has been proposed that not only oxidative stress is a significant early event in the development of the disease, but also it plays an important role in modulating signaling pathways leading to cell death. Recent evidence has suggested that the presence of -amyloid is crucial in the development of the pathology. A results from the sequential proteolysis of the amyloid precursor protein (A PP) by -secretase (BACE1) and -secretase, a multiprotein complex. While, under physiological conditions, A appears to be unfolded, in pathological conditions, it is proposed that it increases the production of amyloid or its ability to aggregate [2, 3]. A toxicity is dependent on A ¡¯s conformational state, peptide length, and concentration [4¨C8]. A deposition in the brain occurs not only in the
%U http://www.hindawi.com/journals/omcl/2014/497802/