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Article type: Short Communication
Authors: Zhang, Chenga; b; * | Rissman, Robert A.a | Feng, Juneb; c
Affiliations: [a] Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA | [b] Department of Biomedical Engineering, Louisiana Tech University, Ruston, LA, USA | [c] Division of Technology, Engineering and Mathematics, Bossier Parish Community College, Bossier City, LA, USA
Correspondence: [*] Correspondence to: Cheng Zhang, Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA. Tel.: +1 858 822 2525; Fax: +1 858 246 0139; E-mail: chz002@ucsd.edu.
Abstract: Mitochondrial impairment as evidenced by decline in adenosine 5′-triphosphate (ATP) is associated with oxidative stress in Alzheimer's disease neuropathology and suggests that mitochondria may fail to maintain cellular energy, through reduced ATP production in neurons. To gain insights into the ATP characteristics of Alzheimer's disease transgenic (Tg) mice, we investigated ATP contents in the brain and whole blood of Tg mice at three ages (1-, 5-, and 24-months old). Overall, our results demonstrate that tissue ATP contents in Tg mice are significantly reduced, suggesting a decrease of tissue ATP production and mitochondrial dysfunction.
Keywords: Adenosine 5′-triphosphate (ATP) contents, Alzheimer's disease, Alzheimer's disease transgenic mouse model, oxidative stress
DOI: 10.3233/JAD-141890
Journal: Journal of Alzheimer's Disease, vol. 44, no. 2, pp. 375-378, 2015
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