TDP-43 gains function due to perturbed autoregulation in a Tardbp knock-in mouse model of ALS-FTD.

doi:10.1038/s41593-018-0113-5

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Article

TDP-43 gains function due to perturbed autoregulation in a Tardbp knock-in mouse model of ALS-FTD.

Nature neuroscience - 1 Apr 2018

White Matthew A, Kim Eosu, Duffy Amanda, Adalbert Robert, Phillips Benjamin U, Peters Owen M, Stephenson Jodie, Yang Sujeong, Massenzio Francesca, Lin Ziqiang, Andrews Simon, Segonds-Pichon Anne, Metterville Jake, Saksida Lisa M, Mead Richard, Ribchester Richard R, Barhomi Youssef, Serre Thomas, Coleman Michael P, Fallon Justin R, Bussey Timothy J, Brown Robert H, Sreedharan Jemeen

Abstract excerpt

Amyotrophic lateral sclerosis-frontotemporal dementia (ALS-FTD) constitutes a devastating disease spectrum characterized by 43-kDa TAR DNA-binding protein (TDP-43) pathology. Understanding how TDP-43 contributes to neurodegeneration will help direct therapeutic efforts. Here we have created a TDP-43 knock-in mouse with a human-equivalent mutation in the endogenous mouse Tardbp gene. TDP-43Q331K mice demonstrate...

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PMID: 29556029
DOI: 10.1038/s41593-018-0113-5
PMCID: PMC5884423

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