C
Christina M. Lang
Researcher at Ludwig Maximilian University of Munich
Publications - 4
Citations - 495
Christina M. Lang is an academic researcher from Ludwig Maximilian University of Munich. The author has contributed to research in topics: Frontotemporal lobar degeneration & Endosome. The author has an hindex of 4, co-authored 4 publications receiving 416 citations.
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Journal ArticleDOI
Common pathobiochemical hallmarks of progranulin-associated frontotemporal lobar degeneration and neuronal ceroid lipofuscinosis
Julia K. Götzl,Julia K. Götzl,Kohji Mori,Markus Damme,Katrin Fellerer,Sabina Tahirovic,Gernot Kleinberger,Jonathan Janssens,Julie van der Zee,Christina M. Lang,Elisabeth Kremmer,Jean-Jacques Martin,Sebastiaan Engelborghs,Hans A. Kretzschmar,Thomas Arzberger,Thomas Arzberger,Christine Van Broeckhoven,Christian Haass,Christian Haass,Anja Capell +19 more
TL;DR: The findings suggest that lysosomal storage disorders and GRN-associated FTLD may share common features and some NCL patients accumulate pathologically phosphorylated TDP-43 within their brains.
Journal ArticleDOI
The FTLD risk factor TMEM106B and MAP6 control dendritic trafficking of lysosomes
Benjamin M. Schwenk,Christina M. Lang,Sebastian Hogl,Sabina Tahirovic,Denise Orozco,Kristin Rentzsch,Stefan F. Lichtenthaler,Stefan F. Lichtenthaler,Casper C. Hoogenraad,Anja Capell,Christian Haass,Christian Haass,Dieter Edbauer,Dieter Edbauer +13 more
TL;DR: This work shows that TMEM106B knockdown in primary neurons affects lysosomal trafficking and blunts dendritic arborization, and identifies microtubule‐associated protein 6 (MAP6) as novel interacting protein for TMEM 106B.
Journal ArticleDOI
Membrane orientation and subcellular localization of transmembrane protein 106B (TMEM106B), a major risk factor for frontotemporal lobar degeneration
Christina M. Lang,Katrin Fellerer,Benjamin M. Schwenk,Peer-Hendrik Kuhn,Elisabeth Kremmer,Dieter Edbauer,Anja Capell,Christian Haass,Christian Haass +8 more
TL;DR: Interestingly, the inhibition of vacuolar H+-ATPases significantly increased the levels of TMEM106B, a finding that may provide an unexpected biochemical link to GRN, because this protein is also strongly increased under the same conditions.
Journal ArticleDOI
Impaired protein degradation in FTLD and related disorders.
TL;DR: The strongest evidence for lysosomal impairment in FTD is provided by the progranulin (GRN) gene, which is linked to FTD and neuronal ceroid lipofuscinosis, and a hypothesis how the interplay of altered nuclear transport and protein degradation leads to the accumulation of protein deposits is provided.