Early temporal short-term memory deficits in double transgenic APP/PS1 mice.

Saioa Lagadec, Lolita Rotureau, Agnès Hémar, Nathalie Macrez, Sebastien Delcasso, Yannick Jeantet, Yoon H. Cho
Neurobiology of Aging. 2012-01-01; 33(1): 203.e1-203.e11
DOI: 10.1016/j.neurobiolaging.2010.07.023

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1. Neurobiol Aging. 2012 Jan;33(1):203.e1-11. doi:
10.1016/j.neurobiolaging.2010.07.023. Epub 2010 Sep 2.

Early temporal short-term memory deficits in double transgenic APP/PS1 mice.

Lagadec S(1), Rotureau L, Hémar A, Macrez N, Delcasso S, Jeantet Y, Cho YH.

Author information:
(1)CNIC, CNRS UMR 5228, Université Bordeaux 1, France.

We tested single APP (Tg2576) transgenic, PS1 (PS1dE9) transgenic, and double
APP/PS1 transgenic mice at 3 and 6 months of age on the acquisition of a
hippocampal-dependent operant “differential reinforcement of low rate schedule”
(DRL) paradigm. In this task mice are required to wait for at least 10 seconds
(DRL-10s) between 2 consecutive nose poke responses. Our data showed that while
single APP and PS1 transgene expression did not affect DRL learning and
performance, mice expressing double APP/PS1 transgenes were impaired in the
acquisition of DRL-10s at 6 months, but not at 3 months of age. The same impaired
double transgenic mice, however, were perfectly capable of normal acquisition of
signaled DRL-10s (SDRL-10s) task, a hippocampal-independent task, wherein mice
were required to emit responses when the end of the 10-second delay was signaled
by a lighting of the chamber. The age-dependent and early deficits of APP/PS1
mice suggest that the appetitive DRL paradigm is sensitive to the amyloid
pathology present in double APP/PS1 mice, and that this mouse line represents a
good model with which to study the efficacy of therapeutic strategies against
Alzheimer’s disease.

Copyright © 2012 Elsevier Inc. All rights reserved.

DOI: 10.1016/j.neurobiolaging.2010.07.023
PMID: 20817351 [Indexed for MEDLINE]

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