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Oxidative Medicine and Cellular Longevity
Volume 2015 (2015), Article ID 509654, 12 pages
Review Article

Mitochondrial Dysfunction Contributes to the Pathogenesis of Alzheimer’s Disease

1Laboratory of Neurodegenerative Diseases, Centro de Investigación Biomédica, Universidad Autónoma de Chile, San Miguel, 8900000 Santiago, Chile
2Departamento de Kinesiología, Universidad Metropolitana de Ciencias de la Educación, Ñuñoa, 7760197 Santiago, Chile

Received 17 March 2015; Revised 9 June 2015; Accepted 18 June 2015

Academic Editor: Matthew C. Zimmerman

Copyright © 2015 Fabian A. Cabezas-Opazo 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 neurodegenerative disease that affects millions of people worldwide. Currently, there is no effective treatment for AD, which indicates the necessity to understand the pathogenic mechanism of this disorder. Extracellular aggregates of amyloid precursor protein (APP), called Aβ peptide and neurofibrillary tangles (NFTs), formed by tau protein in the hyperphosphorylated form are considered the hallmarks of AD. Accumulative evidence suggests that tau pathology and Aβ affect neuronal cells compromising energy supply, antioxidant response, and synaptic activity. In this context, it has been showed that mitochondrial function could be affected by the presence of tau pathology and Aβ in AD. Mitochondria are essential for brain cells function and the improvement of mitochondrial activity contributes to preventing neurodegeneration. Several reports have suggested that mitochondria could be affected in terms of morphology, bioenergetics, and transport in AD. These defects affect mitochondrial health, which later will contribute to the pathogenesis of AD. In this review, we will discuss evidence that supports the importance of mitochondrial injury in the pathogenesis of AD and how studying these mechanisms could lead us to suggest new targets for diagnostic and therapeutic intervention against neurodegeneration.