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

Publication date: 15 January 2018
Source:Behavioural Brain Research, Volume 336
Author(s): Lauren S. Whyte, Kim M. Hemsley, Adeline A. Lau, Sofia Hassiotis, Takashi Saito, Takaomi C. Saido, John J. Hopwood, Timothy J. Sargeant
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 App^NL−F and App^NL−G−F mice. This study aimed to further characterise the behavioural phenotype and amyloid plaque distribution of App^{NL−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 App^{NL−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 App^{NL−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 App^{NL−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 App^{NL−G−F/NL−G−F} knock-in brain.



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