| Abstract No.: | B-C2076 |
| Country: | Canada |
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| Title: | LONGITUDINAL ANALYSIS OF AGE-RELATED BEHAVIORAL CHANGES IN A DOUBLE TRANSGENIC (APPSWE/PS1DE9) MOUSE MODEL OF ALZHEIMER’S DISEASE |
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| Authors/Affiliations: | 1 Jennifer Covey; 1 Rhian Gunn; 1 Richard Brown*;
1 Dalhousie University, Halifax, NS, Canada
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| Content: | Objective: We wished to evaluate a double transgenic mouse model of Alzheimer’s disease in tests of anxiety, learning and memory with age to asses its validity.
Methods: Behavioural analysis of in the B6C3-Tg(APPSwePSEN1dE9)85Dbo/J (APP+PS1dE9) (JAX#004462) transgenic mouse model of Alzheimer's disease (n = 10) and their wild-type littermates (n = 10) was completed at 4, 8, 12, 16 and 20 months of age using a behavioural test battery which included the open field, novel object recognition, accelerating Rotarod, Morris water maze, and passive avoidance. Genotyping was performed by PCR on ear punch samples and body weights were measured at each age.
Results: No significant genotype differences were found in anxiety or locomotion in the open field, but there was a significant decline in activity across age. Transgenic mice showed deficits in the novel object recognition task at twelve months of age. No significant differences were found in motor learning on the Rotarod, but transgenic mice had worse performance than wild-type mice and there was a significant decline in performance across age. In the Morris water maze test for spatial memory, transgenic mice took significantly longer to locate the hidden platform during acquisition learning at sixteen months of age and reversal learning at twenty months of age. Transgenic mice also spent less time in the correct quadrant during the probe trial at four months of age. No genotype differences were found in the passive avoidance test. Body weight in all mice significantly increased with age.
Conclusions: Despite having amyloid plaques forming at 6 - 8 months of age (Burgess et al., 2006, Neurobiol Dis, 24:114-27), we did not find any overt behavioural deficits in these mice by twenty months of age. It is possible that the longitudinal nature of the study provided enrichment so that amyloid plaque deposition was delayed and performance did not decline as expected or that the tasks were not difficult enough to show genotype differences. There were some minor differences in the Morris water maze which may become greater at twenty-four months of age.
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