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.
journal_name
Neurobiol Learn Memjournal_title
Neurobiology of learning and memoryauthors
Masuda A,Kobayashi Y,Kogo N,Saito T,Saido TC,Itohara Sdoi
10.1016/j.nlm.2016.07.001subject
Has Abstractpub_date
2016-11-01 00:00:00pages
73-82eissn
1074-7427issn
1095-9564pii
S1074-7427(16)30101-0journal_volume
135pub_type
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