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Cognitive deficits in single App knock-in mouse models.
- Source :
-
Neurobiology of Learning & Memory . Nov2016, Vol. 135, p73-82. 10p. - Publication Year :
- 2016
-
Abstract
- Transgenic mouse models of Alzheimer’s disease (AD) with nonphysiologic overexpression of amyloid precursor protein (APP) exhibit various unnatural symptoms/dysfunctions. To overcome this issue, mice with single humanized App knock-in (KI) carrying Swedish (NL), Beyreuther/Iberian (F), and Arctic (G) mutations in different combinations were recently developed. The validity of these mouse models of AD from a behavioral viewpoint, however, has not been extensively evaluated. Thus, using an automated behavior monitoring system, we analyzed various behavioral domains, including executive function, and learning and memory. The App -KI mice carrying NL-G-F mutations showed clear deficits in spatial memory and flexible learning, enhanced compulsive behavior, and reduced attention performance. Mice carrying NL-F mutations exhibited modest abnormalities. The NL-G-F mice had a greater and more rapid accumulation of Aβ deposits and glial responses. These findings reveal that single pathologic App -KI is sufficient to produce deficits in broad cognitive domains and that App- KI mouse lines with different levels of pathophysiology are useful models of AD. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 10747427
- Volume :
- 135
- Database :
- Academic Search Index
- Journal :
- Neurobiology of Learning & Memory
- Publication Type :
- Academic Journal
- Accession number :
- 118496514
- Full Text :
- https://doi.org/10.1016/j.nlm.2016.07.001