期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 51, 期 2, 页码 571-580出版社
IOS PRESS
DOI: 10.3233/JAD-150917
关键词
A beta accumulation; cognitive function; mitochondrial dysfunction; oxidative stress
资金
- National Institute of Health
- NSF Chemical Instrumentation Grant [0946883]
- NATIONAL CANCER INSTITUTE [R01CA102264] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS089116] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R37AG037319, R01AG044793] Funding Source: NIH RePORTER
Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized clinically by cognitive decline and memory loss. The pathological features are amyloid-beta peptide (A beta) plaques and intracellular neurofibrillary tangles. Many studies have suggested that oxidative damage induced by reactive oxygen species (ROS) is an important mechanism for AD progression. Our recent study demonstrated that oxidative stress could further impair mitochondrial function. In the present study, we adopted a transgenic mouse model of AD (mAPP, overexpressing A beta PP/A beta in neurons) and performed redox measurements using in vivo electron paramagnetic resonance (EPR) imaging with methoxycarbamyl-proxyl (MCP) as a redox-sensitive probe for studying oxidative stress in an early stage of pathology in a transgenic AD mouse model. Through assessing oxidative stress, mitochondrial function and cognitive behaviors of mAPP mice at the age of 8-9 months, we found that oxidative stress and mitochondrial dysfunction appeared in the early onset of AD. Increased ROS levels were associated with defects of mitochondrial and cognitive dysfunction. Notably, the in vivo EPR method offers a unique way of assessing tissue oxidative stress in living animals under noninvasive conditions, and thus holds a potential for early diagnosis and monitoring the progression of AD.
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