The AD Amyloid Beta-peptide (1-40) is characterized by senile plaques containing β-amyloid peptide (Aβ) derived from the amyloid precursor protein (APP), and by neurofibrillary tangles containing hyperphosphorylated microtubule-associated protein tau [30]. Transgenic mouse models of AD are valuable tools for assessing potential biomarkers as well as for evaluating new therapeutic strategies [31]. This model used in the present study is widely accepted as an accurate model of AD and gives rise to Aβ amyloidosis similar to that found in AD brain. Previous work by our group and by others [32] has revealed age-dependent accumulation of Aβ plaques in cortex and hippocampus, with early onset of Aβ deposition in brain by about 6 mo of age and increased deposition by 12 mo. This work also confirmed the anti-proliferative effects of Aβ on the neural precursor cells [24]. BrdU labeling revealed that proliferative cells were significantly less abundant in the granule cell layer and hilus of the dentate gyrus compared with non-transgenic littermates. The finding of decreased neurogenesis in this transgenic model is consistent with findings made in other mouse AD models.