Alzheimer’s Disease (AD) is a debilitating illness that affects millions of Americans each year. While there is not one definitive hypothesis that exists regarding how the disease develops, some hypotheses include the cholinergic model, the amyloid beta hypothesis, and the tau pathology model. The rTg4510 (Tg) mouse is a model of AD that over-expresses inducible human mutant tau (P301L), a pathological hallmark of AD. This study characterizes the Tg mouse through analysis of adult neurogenesis in the olfactory system, due to the fact that the olfactory system is one of the first sensory systems of the brain to be affected by AD. For this, we examined the behavioral changes in different age groups, specifically 2 and 7 months. Adult neurogenesis within the granule cell layers and glomerular layers in the main and accessory olfactory bulb was analyzed by methods of immunohistochemistry using appropriate antibodies and cell counting with confocal microscopy. Several behavioral paradigms, such as habituation/dishabituation, odor detection threshold, and novel object recognition, were executed to assess cognitive function of these mice, especially in relation to markers of olfactory behavior. Our data suggest that there is an age-dependent cognitive impairment but an age-dependent increase in neurogenesis. Further study is required to identify the effects of inducing the mutant tau on neurogenesis in the olfactory bulb (OB) and whether the overexpression of tau directly impacts cognitive decline.