期刊
FRONTIERS IN AGING NEUROSCIENCE
卷 6, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fnagi.2014.00010
关键词
chronic cerebral hypoperfusion; Alzheimer's disease; cognitive impairment; O-GlcNAcylation; tau phosphorylation; synaptic plasticity markers; brain insulin signaling; neurodegeneration
资金
- First Hospital of Jilin University, China
- New York State Office for People with Developmental Disabilities
- National Natural Science Foundation of China [81000496]
- U.S. Alzheimer's Association [IIRG-10-170405]
Chronic cerebral hypoperfusion (CCH) is one of the causes of vascular dementia (VaD) and is also an etiological factor for Alzheimer's disease (AD). However, how CCH causes cognitive impairment and contributes to Alzheimer's pathology is poorly understood. Here we produced a mouse model of CCH by unilateral common carotid artery occlusion (UCCAO) and studied the behavioral changes and brain abnormalities in mice 2.5 months after UCCAO. We found that CCH caused significant short-term memory deficits and mild longterm spatial memory impairment, as well as decreased level of protein O-GIcNAcylation, increased level of tau phosphorylation, dysregulated synaptic proteins and insulin signaling, and selective neurodegeneration in the brain. These findings provide mechanistic insight into the effects of CCH on memory and cognition and the likely link between AD and VaD.
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