The field has identified

that adult neurogenesis occurs in at least these two regions in rodents through nonhuman primates (e.g., Imayoshi et al., 2008 and Kornack and Rakic, 2001) and in human dentate gyrus as assessed directly using BrdU in cancer patients (Eriksson et al., 1998). Adult neurogenesis in the OB and dentate gyrus has been increasingly implicated in, and demonstrated to function in, olfactory and spatial learning and memory, respectively. Connections to learning and memory make these processes especially interesting, for at least two distinct sets of reasons. CB-839 molecular weight First, because of the core puzzle of how brain circuitry modifies itself with learning—at the levels of molecular changes, synaptic spine changes, connectivity changes, and even via insertion of new neurons by adult neurogenesis. The second is that adult neurogenesis, and reductions thereof, have been implicated in many human disease states (with varying levels of supporting data and plausibility), from major affective psychiatric disease, to neurodegenerative diseases like Alzheimer’s and Parkinson’s diseases, selleck chemicals to drug abuse and addiction. Thus, adult neurogenesis, and by its central place in that field, adult

OB neurogenesis, have assumed positions that are seen to touch upon much broader issues of learning, memory, cognition, plasticity, disease, regeneration, and—yes—even the question of our uniqueness as humans with regard to mental complexity and function. There has been a relatively recent controversy about whether all the deeply interesting results in the field regarding OB neurogenesis in rodents are even relevant in humans. Does the rostral migratory stream (RMS) through which newborn OB neurons migrate in rodents ADP ribosylation factor through nonhuman primates even exist in humans? Is there evidence of continued neuroblast migration through an RMS in postmortem

human brains? Does that reduce to a trickle or less in adult humans? There is compelling evidence that this system is smaller, different in form, and substantially reduced after infancy (Sanai et al., 2004 and Sanai et al., 2011), but work by others indicates that, though its anatomy is altered by brain expansion, a functional RMS exists (Curtis et al., 2007 and Wang et al., 2011). Other work identifies some progenitors directly within the OB itself, perhaps an additional local source for human adult OB neurogenesis (Pagano et al., 2000). Taken together, the system in humans appears different to some or great extent, but is it unique? Does it function at all? In this issue of Neuron, Bergmann et al. (2012) report that adult human OB neurogenesis with long-term neuronal survival is extremely limited … at least in a limited cohort of Swedes, many of whom with neuropsychiatric disease and substance abuse. The authors apply state-of-the-art approaches of 14C cell birth dating that their labs developed several years ago ( Spalding et al.