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Low Dose Pioglitazone Attenuates Oxidative Damage in Early Alzheimer's Disease by Binding mitoNEET: Transcriptome-To-Reactome™ Biosimulation of Neurons

Low Dose Pioglitazone Attenuates Oxidative Damage in Early Alzheimer's Disease by Binding mitoNEET: Transcriptome-To-Reactome™ Biosimulation of Neurons

Charles D. Hammack, George Perry, Richard G. LeBaron, Greg Villareal, Clyde F. Phelix
Copyright: © 2015 |Volume: 5 |Issue: 1 |Pages: 22
ISSN: 1947-9115|EISSN: 1947-9123|EISBN13: 9781466678071|DOI: 10.4018/IJKDB.2015010103
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MLA

Hammack, Charles D., et al. "Low Dose Pioglitazone Attenuates Oxidative Damage in Early Alzheimer's Disease by Binding mitoNEET: Transcriptome-To-Reactome™ Biosimulation of Neurons." IJKDB vol.5, no.1 2015: pp.24-45. http://doi.org/10.4018/IJKDB.2015010103

APA

Hammack, C. D., Perry, G., LeBaron, R. G., Villareal, G., & Phelix, C. F. (2015). Low Dose Pioglitazone Attenuates Oxidative Damage in Early Alzheimer's Disease by Binding mitoNEET: Transcriptome-To-Reactome™ Biosimulation of Neurons. International Journal of Knowledge Discovery in Bioinformatics (IJKDB), 5(1), 24-45. http://doi.org/10.4018/IJKDB.2015010103

Chicago

Hammack, Charles D., et al. "Low Dose Pioglitazone Attenuates Oxidative Damage in Early Alzheimer's Disease by Binding mitoNEET: Transcriptome-To-Reactome™ Biosimulation of Neurons," International Journal of Knowledge Discovery in Bioinformatics (IJKDB) 5, no.1: 24-45. http://doi.org/10.4018/IJKDB.2015010103

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Abstract

Oxidative damage (OD) is considered to be a central component in the progression of Alzheimer's disease (AD). 8-hydroxyguanosine (8-OHG), a readily oxidized ribonucleic acid found in AD, was used as a biomarker to investigate the role of OD in the progression of the disease. A disruption in two critical Thioredoxin-Dependent Peroxiredoxin System components, peroxiredoxin-3 (Prx-3) and thioredoxin (Trx), may serve as a source of the increased accumulation of OD observed in AD. We demonstrate that OD, in the form of 8-OHG, was quantitatively most significant during the earliest stage of AD [F (3, 25) = 5.08, p < .01]. A drastic decline in mitochondrial protein levels of Prx-3 [F (3, 25) = 8.74, p. < 01] and Trx [F (3, 25) = 4.33, p. < 05] were also observed across the progression of the disease. We then tested the efficacy of pioglitazone, a thiazolidinedione class drug aimed to delay onset of AD by acting on mitoNEET. Our results showed a significant reduction in the oxidized variant of mitoNEET within the incipient population when a 0.8mg dose was simulated in silico (p = 0.0242; a. < 05).

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