alexa Mitochondria Specific Antioxidants and their Derivatives in the Context of the Drug Development for Neurodegeneration and Cancer
ISSN: 2169-0138

Drug Designing: Open Access
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Research Article

Mitochondria Specific Antioxidants and their Derivatives in the Context of the Drug Development for Neurodegeneration and Cancer

Gjumrakch Aliev1,2*, Hector H Palacios3, Pablo Cacabelos4 and Ramon Cacabelos4
1“GALLY” International Biomedical Research Consulting LLC, San Antonio, TX 78229, USA
2Department of Health Science and Healthcare Administration, University of Atlanta, Atlanta, GA 30360, USA
3Experimental Gerontology Section, Translational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
4EuroEspes Biomedical Research Center, Institute for CNS Disorders and Genomic Medicine & Camilo José Cela University, 15165 Bergondo, La Coruña, Spain
Corresponding Author : Dr. Gjumrakch Aliev
“GALLY” International Biomedical Research Consulting LLC
7733 Louis Pasteur Drive, #328. San Antonio, TX, 78229, USA
Tel: +1(440) 263-7461
E-mail: [email protected]
Received January 26, 2013; Accepted March 09, 2013; Published March 12, 2013
Citation: Aliev G, Palacios HH, Cacabelos P, Cacabelos R, Burzynski G, et al. (2013) Mitochondria Specific Antioxidants and their Derivatives in the Context of the Drug Development for Neurodegeneration and Cancer. Drug Des 2:103. doi:10.4172/2169-0138.1000103
Copyright: © 2013 Aliev G, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 

Abstract

Neurodegeneration and cancer are fast becoming the leading causes of age-associated disability, dementia and ultimately death worldwide. Although oxidative stress has been intensely studied, little analysis has been done in chronic oxidative stress-induced mitochondrial models. In this regard, DNA-overproliferation and/or deletion initiate mitochondrial deregulation causing energy failure, which has been implicated in the pathogenesis of Alzheimer’s disease (AD), tumor growth, and metastasis. In this regard, decline in mitochondrial normal homeostasis during the development and maturation of the neurodegeneration, tumor growth, and/or metastases is characterized by tissue and cellular oxygen deficiency, which leads to subcellular energy defects. In addition, the overexpression of the cascades initiates the formation and release of large amounts of reactive free radicals [mainly nitric oxide (NO)
via the overexpression of NO synthases], which cause the oxidative stress, cellular alterations, and concomitant mitochondrial lesions and decline in normal organ function. The present study explores the intimate, i.e. direct relationship between chronic oxidative stress and mitochondrial damage as a vital life-supporter for cells and/or the microcirculatory systems whose damage occurs before the development of human AD. Our study highlights the effects of chronic oxidative stress-induced mitochondrial DNA over-proliferation and/or deletion and mitochondrial enzyme activities during the development of human AD. Mitochondrial DNA damage also leads to other pathologies, including colorectal cancer in liver metastasis, and malignant brain cancers. We hypothesize that mitochondrial lesions, especially mitochondrial DNA abnormalities, are detrimental to cell viability and thus mitochondrial DNA damage could be used as a new diagnostic tool and/or criterion for the early detection of AD and other diseases. Further extension of this approach will enable us not only for the better understanding of the blood brain barrier (BBB) homeostasis, which most likely plays a key role in the development of AD and some of forms of the cancer, but also for the development of new and more specific treatment strategies.

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