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Mario Lauterbach

German Center for Neurodegenerative Diseases (DZNE)

University of Bonn

Regina-Pacis-Weg 3

Postfach 2220

Bonn, D-53012

Germany

  • University of Bonn

SCHOLARLY PAPERS

1

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Scholarly Papers (1)

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1.

NLRP3-Mediated Glutaminolysis Regulates Microglia in Alzheimer's Disease

Number of pages: 60 Posted: 03 Aug 2022
Roisin McManus, Max P. Komes, Angelika Griep, Francesco Santarelli, Stephanie Schwartz, Juan Ramon Perea, Michelle-Amirah Khalil, Mario Lauterbach, Lea Heinemann, Titus Schlüter, Juan F. Rodriguez Alcazar, Susanne V. Schmidt, Jasper Spitzer, Peri Noori, Alberto Maillo, David Gomez-Cabrero, Jesper Tegnér, Karsten Hiller, Eicke Latz and Michael T. Heneka
German Center for Neurodegenerative Diseases (DZNE), German Center for Neurodegenerative Diseases (DZNE), German Center for Neurodegenerative Diseases (DZNE), German Center for Neurodegenerative Diseases (DZNE), University of Bonn - Institute of Innate Immunity, German Center for Neurodegenerative Diseases (DZNE), Technology University of Braunschweig - Department of Bioinformatics and Biochemistry, German Center for Neurodegenerative Diseases (DZNE), German Center for Neurodegenerative Diseases (DZNE), German Center for Neurodegenerative Diseases (DZNE), University of Bonn - Institute of Innate Immunity, University of Bonn - Institute of Innate Immunity, University of Bonn - Institute of Innate Immunity, Karolinska Institutet - Computational Medicine Unit, Universidad Pública de Navarra - Translational Bioinformatics Unit, King Abdullah University of Science and Technology (KAUST) - Biological and Environmental Science and Engineering Division, King Abdullah University of Science and Technology (KAUST) - Biological and Environmental Science and Engineering Division, Technology University of Braunschweig - Department of Bioinformatics and Biochemistry, German Center for Neurodegenerative Diseases (DZNE) and University of Bonn - Institute of Innate Immunity
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Citation 6

Abstract:

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Microglia, Alzheimer's disease, NLRP3, inflammasome, glutaminolysis, α-ketoglutarate, phagocytosis, amyloid-β