To the extent that animal models can represent the human condition, this paper argues against a direct connection between changes in Nrg1/ErbB function and the glial hypothesis that is based on postmortem evidence implicating Nrg1/ErbB3 signaling in the etiology of schizophrenia. However, there is a clear difference from the results in this paper with both data from Taveggia, Salzer et al. (on CNS myelination in Nrg1 heterozygotes) and Corfas and colleagues (in animals in which ErbB function is blocked in oligodendrocytes) that needs resolution before any real conclusion can be made. At this point, I think the basic conclusion is that we have a lot more precise (at the cellular level) work to do before we can make really strong predictions on which disease-associated phenotypes relate to disruptions in normal Nrg1/ErbB signaling.

View all comments by David Talmage