Memory disorders result not only from a failure of inputs to the hippocampus, but also from loss of the dentate granule neurons upon which incoming fibers to the hippocampus synapse, or of the hippocampal pyramidal neurons to which the dentate neurons project. The dentate neuronal population is of particular interest because of its ongoing replacement by new neurons (Altman and Das, 1965; Eriksson et al., 1998) - a process that plays a complex role in both the acquisition and extinction of memories (Kempermann et al., 2015). These new adult dentate neurons arise from subgranular zone progenitors that may be isolated to purity from human tissue (Roy et al., 2000), or generated from PSCs (Yu et al., 2014a). The latter report in particular, which describes the Wnt-dependent production of functional dentate granule neurons from human iPS cells, establishes the possibility of adding new dentate neuronal progenitors to hippocampi rendered dysfunctional by regionally-restricted pathologies (Yu et al., 2014b). These may include such conditions as mesial temporal sclerosis or ischemic neuronal loss following hippocampal hypoperfusion, as may occur following cardiac arrest with prolonged
