期刊
MOLECULAR NEURODEGENERATION
卷 5, 期 -, 页码 -出版社
BMC
DOI: 10.1186/1750-1326-5-46
关键词
-
资金
- Natural Science Foundation of China [30770680]
- Program for New Century Excellent Talents in University [NCET-04-0288]
- China Postdoctoral Science Foundation [2005037008]
- Specialized Research Fund for the Doctoral Program of Higher Education [SRFDP-20060159001]
Background: Although increasing evidence has indicated that brain insulin dysfunction is a risk factor for Alzheimer disease (AD), the underlying mechanisms by which insulin deficiency may impact the development of AD are still obscure. Using a streptozotocin (STZ)-induced insulin deficient diabetic AD transgenic mouse model, we evaluated the effect of insulin deficiency on AD-like behavior and neuropathology. Results: Our data showed that administration of STZ increased the level of blood glucose and reduced the level of serum insulin, and further decreased the phosphorylation levels of insulin receptors, and increased the activities of glycogen synthase kinase-3 alpha/beta and c-Jun N-terminal kinase in the APP/PS1 mouse brain. We further showed that STZ treatment promoted the processing of amyloid-beta (A beta) precursor protein resulting in increased A beta generation, neuritic plaque formation, and spatial memory deficits in transgenic mice. Conclusions: Our present data indicate that there is a close link between insulin deficient diabetes and cerebral amyloidosis in the pathogenesis of AD.
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