Research Article
Increased Oxidative Damage in RNA in Alzheimer’s Disease Progression
Bradley-Whitman MA1 and Lovell MA1,2*1Sanders-Brown Center on Aging and Alzheimer’s Disease Center, University of Kentucky, USA
2Department of Chemistry, University of Kentucky, USA
- *Corresponding Author:
- Mark A Lovell, PhD
Sanders-Brown Center on Aging
University of Kentucky, Lexington, KY 40536, USA
Tel: 859-257-1412 (251)
Fax: 859-323-2866
E-mail: malove2@uky.edu
Received date: September 21, 2013; Accepted date: October 28, 2013; Published date: October 30, 2013
Citation: Bradley-Whitman MA, Lovell MA (2013) Increased Oxidative Damage in RNA in Alzheimer’s Disease Progression. J Anal Bioanal Tech S2:004. doi: 10.4172/2155-9872.S2-004
Copyright: © 2013 Bradley-Whitman MA, 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
Studies of oxidative damage during the progression of Alzheimer’s Disease (AD) suggest a central role in disease pathogenesis. To determine if RNA oxidation increases in the progression of AD levels of oxidized bases from RNA from the superior and middle temporal gyri (SMTG), inferior parietal lobule (IPL), and cerebellum (CER) throughout the progression of AD including subjects with mild cognitive impairment (MCI), preclinical AD (PCAD), late-stage AD (LAD), diseased control (DC) (Frontotemporal Dementia (FTD) and Dementia with Lewy Bodies (DLB)), and agematched normal control subjects (NC) were analyzed by gas chromatography mass spectrometry. Median levels of multiple RNA adducts were significantly (p<0.05) elevated in the SMTG, IPL, and CER in multiple stages of AD and in DC subjects. Elevated levels of 4,6-diamino-5-foramidopyrimidine (FapyA) suggest a hypoxic environment early in the progression of AD and in DC subjects. Overall, these data suggest oxidative damage is an early event not only in the pathogenesis of AD, but is present in neurodegenerative diseases in general.
