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Paper Details

Loss of TMEM106B leads to myelination deficits: implications for frontotemporal dementia treatment strategies.
Brain
37
2020
FTD, FTD-TDP, OLIG2, OLIG2-positive cells, PLP1, TDP, TDP-43, TMEM106B, TMEM106B HeLa knock-out cell line, TMEM106B locus, Tmem106-/-, Tmem106b, Tmem106b+/+, Tmem106b+/-, Tmem106b-/-, cas9, correlated genes, cuprizone, demyelination, frontotemporal dementia, genes, mice, mouse, myelination deficits, neurodegenerative diseases, oligodendrocyte, primary cultured oligodendrocytes, progranulin mutation, undifferentiated oligodendrocytes
Author NameAffiliation
NiCole A FinchMayo Clinic
Yan W AsmannMayo Clinic
Cathleen LutzJAX Center for Precision Genetics
Cathleen LutzJAX Center for Precision Genetics
Dennis W DicksonMayo Clinic
Rosa RademakersMayo Clinic
Rosa RademakersVIB Center for Molecular Neurology, Universiteitsplein 1
Rosa RademakersUniversity of Antwerp, Universiteitsplein 1
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