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Oxidative Medicine and Cellular Longevity
Volume 2013, Article ID 940603, 6 pages
Review Article

Phosphorylation of Tau Protein as the Link between Oxidative Stress, Mitochondrial Dysfunction, and Connectivity Failure: Implications for Alzheimer’s Disease

1Douglas Hospital Research Center, Department of Psychiatry, McGill University, Montreal, QC, Canada H4H 1R3
2UTSA Neurosciences Institute and Department of Biology, College of Sciences, University of Texas at San Antonio, San Antonio, TX 78249, USA
3Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
4Center for Neuroscience and Cell Biology, University of Coimbra, 3000-354 Coimbra, Portugal
5Faculty of Medicine, Institute of Physiology, University of Coimbra, 3000-548 Coimbra, Portugal
6Faculty of Medicine, Université de Montreal, QC, Canada H3C 3J7

Received 11 December 2012; Accepted 6 June 2013

Academic Editor: Grzegorz A. Czapski

Copyright © 2013 Siddhartha Mondragón-Rodríguez 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 defined by the concurrence of abnormal aggregates composed of phosphorylated tau protein and of abnormal cellular changes including neurite degeneration, loss of neurons, and loss of cognitive functions. While a number of mechanisms have been implicated in this complex disease, oxidative stress remains one of the earliest and strongest events related to disease progression. However, the mechanism that links oxidative stress and cognitive decline remains elusive. Here, we propose that phosphorylated tau protein could be playing the role of potential connector and, therefore, that a combined therapy involving antioxidants and check points for synaptic plasticity during early stages of the disease could become a viable therapeutic option for AD treatment.