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Patricia Martín-Maestro [1; 2; 3] and Ricardo Gargini [1] and Esther García [1; 2] and George Perry [4] and Jesús Avila [1; 2] and Vega García-Escudero [1; 2; 5]

Academic Editor: Icksoo Lee

1, Centro de Biología Molecular “Severo Ochoa” (UAM-CSIC), Nicolás Cabrera, 1. Cantoblanco 28049 Madrid, Spain, uam.es

2, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Valderrebollo, 5, 28031 Madrid, Spain, ciberned.es

3, Brain and Mind Research Institute, Weill Cornell Medical College, Cornell University, 407 E 61st St. 1300 York Avenue, New York, NY 10065, USA, cornell.edu

4, University of Texas at San Antonio, One UTSA Circle, San Antonio, TX 78249-0667, USA, utsa.edu

5, Departamento de Anatomía, Histología y Neurociencia, Facultad de Medicina, UAM, Arzobispo Morcillo, 4, 28029 Madrid, Spain, uam.es

Received Mar 31, 2017; Revised Jul 25, 2017; Accepted Aug 17, 2017

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.

1. Introduction

Alzheimer’s disease (AD) is a common and devastating dementia that is pathologically defined by the accumulation of extracellular amyloid beta- (Aβ-) containing plaques and intraneuronal hyperphosphorylated Tau protein aggregates associated with neuronal loss in the cerebral cortex. Studies of whole-genome gene expression profiling have identified that AD patients exhibit mitochondrial impairment together with altered calcium signaling and inflammation [1]. Defects in mitochondrial function generate oxidative stress increase due to mitochondrial electron transport chain leakage. The generated reactive oxygen species (ROS) oxidize multiple cell components, being an important issue to trigger protein misfolding [2]. It has been proposed that oxidative stress could be one of the primary events in the development of AD and plays a pivotal role in its pathogenesis [3, 4]. At the same time, mitochondria are targets of ROS causing the oxidation of their components increasing mitochondrial deterioration. This mitochondrial dysfunction may be one of the earliest and most prominent features of AD [5, 6]. Several works that show downregulation of mitochondrial genes in Alzheimer’s have also demonstrated a reduced metabolic rate in the brain of these patients measured by fluorodeoxyglucose PET [7]. Metabolic abnormalities besides the damage of both components and the structure of mitochondria are well described in AD [8–10]....

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