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Behav Brain Res. 2018 Jan 15;336:177-181. doi: 10.1016/j.bbr.2017.09.006. Epub 2017 Sep 5.

Reduction in open field activity in the absence of memory deficits in the AppNL-G-F knock-in mouse model of Alzheimer's disease.

Author information

1
The University of Adelaide, School of Medicine, North Terrace, Adelaide, Australia; Lysosomal Diseases Research Unit, Nutrition and Metabolism Theme, South Australian Health and Medical Research Institute, North Terrace, Adelaide, Australia.
2
Lysosomal Diseases Research Unit, Nutrition and Metabolism Theme, South Australian Health and Medical Research Institute, North Terrace, Adelaide, Australia.
3
Laboratory for Proteolytic Neuroscience, Brain Science Institute, RIKEN, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan.
4
Lysosomal Diseases Research Unit, Nutrition and Metabolism Theme, South Australian Health and Medical Research Institute, North Terrace, Adelaide, Australia. Electronic address: tim.sargeant@sahmri.com.

Abstract

The recent development of knock-in mouse models of Alzheimer's disease provides distinct advantages over traditional transgenic mouse models that rely on over-expression of amyloid precursor protein. Two such knock-in models that have recently been widely adopted by Alzheimer's researchers are the AppNL-F and AppNL-G-F mice. This study aimed to further characterise the behavioural phenotype and amyloid plaque distribution of AppNL-G-F/NL-G-F (C57BL/6J background) mice at six-months of age. An attempt to replicate a previous study that observed deficits in working memory in the Y-maze, showed no difference between AppNL-G-F/NL-G-F and wild-type mice. Further assessment of these mice using the novel object recognition test and Morris water maze also revealed no differences between AppNL-G-F/NL-G-F and wild-type mice. Despite a lack of demonstrated cognitive deficits, we report a reduction in locomotor/exploratory activity in an open field. Histological examination of AppNL-G-F/NL-G-F mice showed widespread distribution of amyloid plaques at this age. We conclude that whilst at six-months of age, memory deficits are not sufficiently robust to be replicated in varying environments, amyloid plaque burden is significant in AppNL-G-F/NL-G-F knock-in brain.

KEYWORDS:

Alzheimer’s disease; App(NL-G-F); Morris water maze; Y-maze; novel object recognition test; open field

PMID:
28887197
DOI:
10.1016/j.bbr.2017.09.006
[Indexed for MEDLINE]

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