stimulus-specific manner, and contribute to strengthening of memory circuits related to the stimulus given (Trouche et al., 2009). Computational hypotheses have suggested that the turnover of neurons in the DG associated with neurogenesis may provide protection against memory interference when similar items are presented (Becker, 2005; Wiskott et al., 2006). An alternative theory suggests that due to the tendency of newly formed neurons to be easily excitable and more readily undergo long term potentiation, they may be a means by which memories are temporally organized (Aimone et al., 2006). Impairments in neurogenesis may compromise the extent of plasticity of the hippocampus, olfactory system and their associated neural circuits. This could lead to enhanced neuronal vulnerability in these brain areas and functional impairments, such as a reduced capacity for learning and memory. Recent evidence in support of this hypothesis suggests that neurogenesis is impaired in animal models of AD in both SVZ and SGL (Demars et al., 2009). Neurogenic impairments may underlie, at least in part, the progressive loss of memory and compromised ability to learn and process new information characterizing the disease. Both olfactory and hippocampal dysfunction might be enhanced by compromised neurogenesis in the SVZ and SGL of the
