Neurodegenerative diseases are characterized by the gradual loss of functional neuronal populations within the nervous system (Cummings et al., 1998; Jenner & Olanow, 1998; Kowall et al., 1987). While all other organs of the body typically replace lost cells by proliferation and differentiation of resident tissue-specified stem cell populations, the adult central nervous system does not appear capable of regenerating dying neurons to any clinically significant degree. Historically, this inability of the mammalian nervous system to regenerate had led to the conclusion that the adult CNS did not contain competent neuronal progenitor or stem cells. However, a number of studies over the past two decades have refuted this dogma, by identifying significant and heterogeneous populations of both neural stem and progenitor cells in the adult brain (Altman & Das, 1966; Bayer et al., 1982; Goldman & Nottebohm, 1983; Goldman et al., 1992; Kirschenbaum et al., 1994; Lois & Alvarez-Buylla, 1993; Luskin, 1993; Reynolds & Weiss, 1992; Richards et al., 1992). These discoveries have led to the suggestion that induced compensatory neurogenesis by endogenous progenitor cells should be experimentally and therapeutically feasible, regardless of whether compensatory neurogenesis proves to be a natural occurrence of any clinical significance (Gage, 2000; Goldman et al., 2002; Goldman & Luskin, 1998; Weiss et al., 1996b).