Edbauer, Dieter
https://orcid.org/0000-0002-7186-4653
Mayo Clinic
German Center for Neurodegenerative Diseases
Citations 1
C9ORF72 repeat expansions in mice cause TDP-43 pathology, neuronal loss, and behavioral deficits
Chew, Jeannie , Prudencio, Mercedes , Sasaguri, Hiroki , Zhang, Yong‐Jie , Castanedes‐Casey, Monica , Lee, Chris W. , Jansen‐West, Karen , Kurti, Aishe, Murray, Melissa E. , Bieniek, Kevin F. , Bauer, Peter , Whitelaw, Ena C., Rousseau, Linda , Stankowski, Jeannette N. , Stetler, Caroline, Daughrity, Lillian M. , Perkerson, Emilie A., Desaro, Pamela , Johnston, Amelia, Overstreet, Karen, Edbauer, Dieter , Rademakers, Rosa , Fryer, John Denis , Petrucelli, Leonard , Gendron, Tania F. , Castanedes-Casey, Monica, Jansen-West, Karen, Bauer, Peter O, Boylan, Kevin B, Fryer, John D., Boylan, Khrista , Dickson, Dennis W. , Zhang, Yong-Jie , Prudencio, Mercedes , Murray, Melissa E
Science | May 14, 2015 | Volume: 348 | Issue: 6239 | Pages: 1151-1154
A mouse model for ALS A G4C2 repeat expansion in C9ORF72 is known to be the major genetic cause of frontotemporal dementia and amyotrophic lateral sclerosis (c9FTD/ALS). However, a lack of animal models recapitulating key disease features has hindered efforts to understand and prevent c9FTD/ALS-related neurodegeneration. Until now. Chew et al. describe a mouse model that mimics both neuropathological and clinical phenotypes of c9FTD/ALS. Science , this issue p. 1151