期刊
PROTEOMICS
卷 11, 期 21, 页码 4243-4256出版社
WILEY
DOI: 10.1002/pmic.201000523
关键词
APP/PS1; Alzheimer disease; Animal proteomics; Mild cognitive impairment; N-Acetylcysteine; Oxidative stress; Protein oxidation
资金
- NIH [AG-10836, AG-05119]
- University of Kentucky
- UNCF-Merck Science Initiative
Proteomics analyses were performed on the brains of wild-type (WT) controls and an Alzheimer's disease (AD) mouse model, APP/PS-1 human double mutant knock-in mice. Mice were given either drinking water or water supplemented with N-acetylcysteine (NAC) (2 mg/kg body weight) for a period of five months. The time periods of treatment correspond to ages prior to A beta deposition (i.e. 4-9 months), resembling human mild cognitive impairment (MCI), and after A beta deposition (i.e. 7-12 months), more closely resembling advancing stages of AD. Substantial differences exist between the proteomes of WT and APP/PS-1 mice at 9 or 12 months, indicating that A beta deposition and oxidative stress lead to downstream changes in protein expression. Altered proteins are involved in energy-related pathways, excitotoxicity, cell cycle signaling, synaptic abnormalities, and cellular defense and structure. Overall, the proteomic results support the notion that NAC may be beneficial for increasing cellular stress responses in WT mice and for influencing the levels of energy-and mitochondria-related proteins in APP/PS-1 mice.
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