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Oxidative Medicine and Cellular Longevity
Volume 2013, Article ID 962984, 19 pages
http://dx.doi.org/10.1155/2013/962984
Review Article

Link between Cancer and Alzheimer Disease via Oxidative Stress Induced by Nitric Oxide-Dependent Mitochondrial DNA Overproliferation and Deletion

1GALLY International Biomedical Research Consulting LLC, 7733 Louis Pasteur Drive, No. 328, San Antonio, TX 78229, USA
2School of Health Science and Healthcare Administration, The University of Atlanta, 6685 Peachtree Industrial Boulevard, Atlanta, GA 30360, USA
3Departments of Chemistry and Biology, Cleveland State University, 10701 East Boulevard, 113-W, Cleveland, OH 44106, USA
4Metabolomics and Enzymology Unit, Fundamental and Applied Biology Group, King Fahd Medical Research Center, King Abdulaziz University, Jeddah 21589, Saudi Arabia
5Department of Chemistry, Missouri University of Science and Technology, 341 Schrenk Hall, Rolla, MO 65409, USA
6Department of Genetics, School of Medicine, Yale University, 333 Cedar Street, New Haven, CT 06520, USA
7Autonomic Neuroscience Institute, Royal Free Hospital School of Medicine, London NW3 2PF, UK
8The Department of Pharmacology, Level 8, Medical Building (No. 181), Corner of Grattan Street and Royal Parade University of Melbourne, Victoria, 3010, Australia
9EuroEspes Biomedical Research Center, Institute for CNS Disorders and Genomic Medicine and Camilo José Cela University, Sta. Marta de Babío, s/n, La Coruña, 15165 Bergondo, Spain

Received 14 December 2012; Accepted 1 February 2013

Academic Editor: Sumitra Miriyala

Copyright © 2013 Gjumrakch Aliev 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.

Abstract

Nitric oxide- (NO-) dependent oxidative stress results in mitochondrial ultrastructural alterations and DNA damage in cases of Alzheimer disease (AD). However, little is known about these pathways in human cancers, especially during the development as well as the progression of primary brain tumors and metastatic colorectal cancer. One of the key features of tumors is the deficiency in tissue energy that accompanies mitochondrial lesions and formation of the hypoxic smaller sized mitochondria with ultrastructural abnormalities. We speculate that mitochondrial involvement may play a significant role in the etiopathogenesis of cancer. Recent studies also demonstrate a potential link between AD and cancer, and anticancer drugs are being explored for the inhibition of AD-like pathology in transgenic mice. Severity of the cancer growth, metastasis, and brain pathology in AD (in animal models that mimic human AD) correlate with the degree of mitochondrial ultrastructural abnormalities. Recent advances in the cell-cycle reentry of the terminally differentiated neuronal cells indicate that NO-dependent mitochondrial abnormal activities and mitotic cell division are not the only important pathogenic factors in pathogenesis of cancer and AD, but open a new window for the development of novel treatment strategies for these devastating diseases.