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Article type: Short Communication
Authors: Wang, Haoa | Hong, Xiaoyua | Wang, Yongb; *
Affiliations: [a] College of Life Sciences and Oceanography, Shenzhen Key Laboratory of Microbial Genetic Engineering, Shenzhen University, Shenzhen, China | [b] College of Life Sciences and Oceanography, Shenzhen Key Laboratory of Marine Bioresources and Ecology, Shenzhen University, Shenzhen, China
Correspondence: [*] Correspondence to: Yong Wang, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen, China. Tel.: +86 137 983 50829; Fax: +86 755 265 34274; E-mail: wyong@szu.edu.cn.
Abstract: Mitochondrial dysfunction plays a pivotal role in Alzheimer’s disease (AD), even before signs of AD pathology are evident. Our previous research has shown that oxygen treatment can improve cognitive function in AD model mice. To address whether oxygen treatment is beneficial to mitochondrial biology, we analyzed differential expressions of hippocampal mitochondrial proteins in AD model mice given supplementary oxygen. Numerous respiratory chain, Kreb’s cycle, and glycolysis proteins were upregulated significantly after oxygen treatment, suggesting that oxygen therapy can alleviate mitochondrial damage. Furthermore, the treatment was associated with decreased expressions of some AD biomarkers, suggesting oxygen treatment to be a potential therapy for AD.
Keywords: Alzheimer’s disease, iTRAQ, mitochondria, oxidative phosphorylation, oxygen, proteomics
DOI: 10.3233/JAD-161010
Journal: Journal of Alzheimer's Disease, vol. 56, no. 3, pp. 875-883, 2017
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