In rodents and humans, neurons newly formed from stem cells in the SVZ migrate to the olfactory bulb and contribute to olfactory function (Alvarez-Buylla & Lim, 2004; Curtis et al. 2007). Innate alcohol preference in mice seems to be strongly dependent on genes with localized expression in the olfactory system (Tabakoff et al. 2008). Deficits in olfactory sensitivity and discrimination specifically related to alcohol dependence have been described repeatedly in humans (Potter & Butters, 1979; Rupp et al. 2003; Rupp et al. 2004). It has recently been found that these impairments correlate with the degree of impairment for executive cognitive function (Rupp et al. 2006), a category of deficit that also predicts relapse in recently detoxified severe alcoholics (Wicks et al. 2001). The biological mechanisms linking SVZ neurogenesis, alcohol preference, olfactory bulb function and executive deficits are presently unknown. However, alcoholics have cognitive deficits that improve in abstinence, but do not completely return to control levels (Crews et al. 2005), consistent with partial but incomplete recovery of neurogenesis. The loss of SVZ progenitors following prolonged alcohol dependence could thus contribute to long-term changes in cognitive function and risk for relapse in abstinent alcoholics.
