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Current Gerontology and Geriatrics Research
Volume 2012 (2012), Article ID 724904, 10 pages
http://dx.doi.org/10.1155/2012/724904
Review Article

Oxidative Stress and Down Syndrome: A Route toward Alzheimer-Like Dementia

1Department of Biochemical Sciences, Faculty of Pharmacy and Medicine, Sapienza University of Rome 00185 Rome, Italy
2Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
3Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA
4Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA

Received 29 July 2011; Revised 10 October 2011; Accepted 11 October 2011

Academic Editor: David Patterson

Copyright © 2012 Marzia Perluigi and D. Allan Butterfield. 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.

Abstract

Down syndrome (DS) is one of the most frequent genetic abnormalities characterized by multiple pathological phenotypes. Indeed, currently life expectancy and quality of life for DS patients have improved, although with increasing age pathological dysfunctions are exacerbated and intellectual disability may lead to the development of Alzheimer's type dementia (AD). The neuropathology of DS is complex and includes the development of AD by middle age, altered free radical metabolism, and impaired mitochondrial function, both of which contribute to neuronal degeneration. Understanding the molecular basis that drives the development of AD is an intense field of research. Our laboratories are interested in understanding the role of oxidative stress as link between DS and AD. This review examines the current literature that showed oxidative damage in DS by identifying putative molecular pathways that play a central role in the neurodegenerative processes. In addition, considering the role of mitochondrial dysfunction in neurodegenerative phenomena, results demonstrating the involvement of impaired mitochondria in DS pathology could contribute a direct link between normal aging and development of AD-like dementia in DS patients.