Intraneuronal β-Amyloid Aggregates, Neurodegeneration, and Neuron Loss in Transgenic Mice with Five Familial Alzheimer's Disease Mutations: Potential Factors in Amyloid Plaque Formation

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Figure 9.
Figure 9.

Memory deficits in Tg6799 mice with age. A, Spatial working memory of Tg6799 and nontransgenic littermate (Wild-type) mice was assessed by spontaneous alternation in the Y-maze (n = 12–20). Tg6799 mice showed normal alternation performance in the Y-maze at 2 months of age, but they performed poorly at 4–5 months of age (only slightly >50% chance levels) compared with nontransgenic littermate mice (F(3,62) = 13.96; p < 0.01). B, The total number of arm entries was not different between Tg6799 and nontransgenic (Wild-type) control mice, indicating similar levels of motor and exploratory activity in the Y-maze (n = 12–21). Each column represents the mean ± SEM. **p < 0.01 versus nontransgenic compared by ANOVA and post hoc Fisher's PLSD test.

  1. The Journal of Neuroscience vol. 26 no. 40 10129-10140
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