Loss of Tmem106b is unable to ameliorate frontotemporal dementia-like phenotypes in an AAV mouse model of C9ORF72-repeat induced toxicity

Loss of Tmem106b is unable to ameliorate frontotemporal dementia-like phenotypes in an AAV mouse model of C9ORF72-repeat induced toxicity

Abstract Loss-of-function mutations in progranulin (GRN) and a non-coding (GGGGCC)n hexanucleotide repeat expansions in C9ORF72 are the two most common genetic causes of frontotemporal lobar degeneration with aggregates of TAR DNA binding protein 43 (FTLD-TDP). TMEM106B encodes a type II transmembra...

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Bibliographic Details
Main Authors: Alexandra M. Nicholson, Xiaolai Zhou, Ralph B. Perkerson, Tammee M. Parsons, Jeannie Chew, Mieu Brooks, Mariely DeJesus-Hernandez, NiCole A. Finch, Billie J. Matchett, Aishe Kurti, Karen R. Jansen-West, Emilie Perkerson, Lillian Daughrity, Monica Castanedes-Casey, Linda Rousseau, Virginia Phillips, Fenghua Hu, Tania F. Gendron, Melissa E. Murray, Dennis W. Dickson, John D. Fryer, Leonard Petrucelli, Rosa Rademakers
Format: Article
Language:English
Published: BMC 2018-05-01
Series:Acta Neuropathologica Communications
Online Access:http://link.springer.com/article/10.1186/s40478-018-0545-x

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http://link.springer.com/article/10.1186/s40478-018-0545-x

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