Nature Communications (Feb 2021)
Loss of NPC1 enhances phagocytic uptake and impairs lipid trafficking in microglia
- Alessio Colombo,
- Lina Dinkel,
- Stephan A. Müller,
- Laura Sebastian Monasor,
- Martina Schifferer,
- Ludovico Cantuti-Castelvetri,
- Jasmin König,
- Lea Vidatic,
- Tatiana Bremova-Ertl,
- Andrew P. Lieberman,
- Silva Hecimovic,
- Mikael Simons,
- Stefan F. Lichtenthaler,
- Michael Strupp,
- Susanne A. Schneider,
- Sabina Tahirovic
Affiliations
- Alessio Colombo
- German Center for Neurodegenerative Diseases (DZNE) Munich
- Lina Dinkel
- German Center for Neurodegenerative Diseases (DZNE) Munich
- Stephan A. Müller
- German Center for Neurodegenerative Diseases (DZNE) Munich
- Laura Sebastian Monasor
- German Center for Neurodegenerative Diseases (DZNE) Munich
- Martina Schifferer
- Munich Cluster for Systems Neurology (SyNergy)
- Ludovico Cantuti-Castelvetri
- German Center for Neurodegenerative Diseases (DZNE) Munich
- Jasmin König
- German Center for Neurodegenerative Diseases (DZNE) Munich
- Lea Vidatic
- Division of Molecular Medicine, Ruder Boskovic Institute
- Tatiana Bremova-Ertl
- Department of Neurology, Ludwig-Maximilians University
- Andrew P. Lieberman
- Department of Pathology, University of Michigan
- Silva Hecimovic
- Division of Molecular Medicine, Ruder Boskovic Institute
- Mikael Simons
- German Center for Neurodegenerative Diseases (DZNE) Munich
- Stefan F. Lichtenthaler
- German Center for Neurodegenerative Diseases (DZNE) Munich
- Michael Strupp
- Department of Neurology, Ludwig-Maximilians University
- Susanne A. Schneider
- Department of Neurology, Ludwig-Maximilians University
- Sabina Tahirovic
- German Center for Neurodegenerative Diseases (DZNE) Munich
- DOI
- https://doi.org/10.1038/s41467-021-21428-5
- Journal volume & issue
-
Vol. 12,
no. 1
pp. 1 – 20
Abstract
Niemann-Pick type C disease is a rare childhood neurodegenerative disorder predominantly caused by mutations in NPC1, resulting in abnormal late endosomal and lysosomal defects. Here the authors show that NPC1 disruption largely impairs microglial function.
