Journal
LEARNING & MEMORY
Volume 8, Issue 6, Pages 301-308Publisher
COLD SPRING HARBOR LAB PRESS
DOI: 10.1101/lm.43701
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Funding
- NIA NIH HHS [AG15453] Funding Source: Medline
- NINDS NIH HHS [NS33249] Funding Source: Medline
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Recent advances in behavioral analyses of transgenic mouse models of Alzheimer's disease (AD) are discussed, and their impact on our understanding of the molecular basis of cognitive impairment in AD is considered. Studies of the relationship between memory and Abeta in transgenic mice expressing the amyloid precursor protein (APP) and its variants suggest that aging promotes the formation of soluble AB assemblies mediating negative effects on memory. A significant component of memory loss in APP transgenic mice is apparently caused by soluble Abeta assemblies, but whether and how much of the dementia within individuals afflicted with AD is caused by these AB species is unclear. Future studies in composite transgenic mice developing amyloid plaques, neurofibrillary tangles, and other AD pathology may allow for the determination of the relative contribution of AB and non-Abeta components to dementia.
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