Suzuki, NaokiMaroof, AsifMerkle, FlorianKoszka, KathrynIntoh, AtsushiArmstrong, IanMoccia, RobDavis-Dusenbery, Brandi NEggan, Kevin2015-05-042014Suzuki, Naoki, Asif Maroof, Florian T Merkle, Kathryn Koszka, Atsushi Intoh, Ian Armstrong, Rob Moccia, Brandi N Davis-Dusenbery, and Kevin Eggan. 2014. “The mouse C9ORF72 ortholog is enriched in neurons known to degenerate in ALS and FTD.” Nature neuroscience 16 (12): 1725-1727. doi:10.1038/nn.3566. http://dx.doi.org/10.1038/nn.3566.1097-6256http://nrs.harvard.edu/urn-3:HUL.InstRepos:15034763Using transgenic animals harboring a targeted LacZ insertion, we studied the expression pattern of the C9ORF72 mouse ortholog. Unlike most genes mutated in ALS, which are ubiquitously expressed, the C9ORF72-ortholog was most highly transcribed in the neuronal populations sensitive to degeneration in ALS and FTD. Thus, our study provides a potential explanation for the cell type specificity of neuronal degeneration caused by C9ORF72 mutations.en-USAmyotrophic lateral sclerosis (ALS)frontotemporal dementia (FTD)C9ORF72motor neuroncortical neuronhippocampusastrocytemicroglialJournal Article2015-05-0410.1038/nn.3566