Two recent papers have attracted a lot of media attention because they draw direct links between adult neurogenesis and behavioral disorders: Noonan et al. showed that rats lacking adult neurogenesis (stopped with irradiation) are more susceptible to cocaine addiction. Jin et al. showed that mice lacking adult neurogenesis (using a transgenic model) suffer greater infarct size and have more severe motor deficits after stroke.
While the papers themselves have important implications, what caught my attention was the angle taken by press releases: both articles studied the effects of reducing neurogenesis but the media focused on potential benefits of increasing neurogenesis. See speculation that antidepressants, by increasing neurogenesis, might be stroke-protective here. And, from Science Daily:
While the research specifically focused on what happens when neurogenesis is blocked, the scientists said the results suggest that increasing adult neurogenesis might be a potential way to combat drug addiction and relapse.
It may very well be the case that increasing neurogenesis is good in the same way decreasing neurogenesis is bad but it shouldn’t be assumed – maybe we have all the neurogenesis we need and, while completely arresting neurogenesis could be harmful, increasing neurogenesis beyond normal levels is just redundant.
Or, maybe the key is where you’re increasing or decreasing neurogenesis from:
In this model, assuming most of us have normal levels of neurogenesis, further increases will provide no benefit to behavioral performance, whether we’re talking resistance to addiction or recovery from stroke or anything else. However, decreases in the number of young neurons below a critical level would impair storing/processing of information, protection against stroke etc.
This speculation is under the assumption that we all have “normal” or sufficiently high levels of constitutive neurogenesis. However, in the case of addiction, covariables like stress, poor nutrition and narcotics themselves might all serve to reduce neurogenesis below healthy levels (see “unhealthy levels” in figure). In this case, increasing neurogenesis would cause dramatic improvements in behavior and is consistent with the authors’ speculation. For similar reasons, increasing neurogenesis might provide cognitive benefits to people in other situations where neurogenesis is known to be compromised: the aged, those experiencing chronic stress, patients undergoing cranial irradiation or chemotherapy.
It may be surprising that this idea is actually very hard to test, even in the laboratory. While many tools exist for reducing neurogenesis to unhealthy levels (irradiation, antimitotic drugs, genetics) there are no tools for selectively increasing neurogenesis beyond normal/healthy levels. Yet.
Noonan MA, Bulin SE, Fuller DC, & Eisch AJ (2010). Reduction of adult hippocampal neurogenesis confers vulnerability in an animal model of cocaine addiction. The Journal of neuroscience : the official journal of the Society for Neuroscience, 30 (1), 304-15 PMID: 20053911
Jin K, Wang X, Xie L, Mao XO, & Greenberg DA (2010). Transgenic ablation of doublecortin-expressing cells suppresses adult neurogenesis and worsens stroke outcome in mice. Proceedings of the National Academy of Sciences of the United States of America PMID: 20385829