In the August 28 Neuron, Se Hoon Choi, Karthikeyan Veeraraghavalu, and colleagues led by Sangram Sisodia at the University of Chicago, Illinois, report a new role for certain presenilin-1 mutations that cause early-onset familial Alzheimer disease (eFAD). Mice transgenic for some of these mutations fail to boost their hippocampal neurogenesis when kept in conditions of environmental enrichment. Interestingly, this deficit is largely mediated by nearby microglia, which, when carrying PS1 mutations, no longer respond to the environmental stimulus by releasing certain soluble signaling factors that are needed for enhanced neurogenesis. If confirmed and expanded, this finding would suggest that familial AD is, in some part, a disease of glial cells. The paper publishes full data of a research project previously reported on Alzforum after the 2007 Society for Neuroscience conference in San Diego, California (see ARF related conference story).—Gabrielle Strobel
- Choi SH, Veeraraghavalu K, Lazarov O, Marler S, Ransohoff RM, Ramirez JM, Sisodia SS. Non-cell-autonomous effects of presenilin 1 variants on enrichment-mediated hippocampal progenitor cell proliferation and differentiation. Neuron. 2008 Aug 28;59(4):568-80. PubMed.