Deutsch
 
Hilfe Datenschutzhinweis Impressum
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT

Freigegeben

Zeitschriftenartikel

Gut microbiota drives age-related oxidative stress and mitochondrial damage in microglia via the metabolite N6-carboxymethyllysine

MPG-Autoren

Mossad,  Omar
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Batut,  Bérénice
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Yilmaz,  Bahtiyar
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Dokalis,  Nikolaos
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Mezö,  Charlotte
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Nent,  Elisa
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Nabavi,  Lara Susann
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Mayer,  Melanie
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Maron,  Feres José Mocayar
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons241896

Büscher,  Jörg Martin
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

de Agüero,  Mercedes Gomez
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Szalay,  Antal
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons204285

Lämmermann,  Tim
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Macpherson,  Andrew J
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Ganal-Vonarburg,  Stephanie C
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Backofen,  Rolf
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Erny,  Daniel
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Prinz,  Marco
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Blank,  Thomas
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Externe Ressourcen
Volltexte (beschränkter Zugriff)
Für Ihren IP-Bereich sind aktuell keine Volltexte freigegeben.
Volltexte (frei zugänglich)
Es sind keine frei zugänglichen Volltexte in PuRe verfügbar
Ergänzendes Material (frei zugänglich)
Es sind keine frei zugänglichen Ergänzenden Materialien verfügbar
Zitation

Mossad, O., Batut, B., Yilmaz, B., Dokalis, N., Mezö, C., Nent, E., et al. (2022). Gut microbiota drives age-related oxidative stress and mitochondrial damage in microglia via the metabolite N6-carboxymethyllysine. Nature Neuroscience, 25, 295-305. doi:10.1038/s41593-022-01027-3.


Zitierlink: https://hdl.handle.net/21.11116/0000-000A-1809-2
Zusammenfassung
Microglial function declines during aging. The interaction of microglia with the gut microbiota has been well characterized during development and adulthood but not in aging. Here, we compared microglial transcriptomes from young-adult and aged mice housed under germ-free and specific pathogen-free conditions and found that the microbiota influenced aging associated-changes in microglial gene expression. The absence of gut microbiota diminished oxidative stress and ameliorated mitochondrial dysfunction in microglia from the brains of aged mice. Unbiased metabolomic analyses of serum and brain tissue revealed the accumulation of N6-carboxymethyllysine (CML) in the microglia of the aging brain. CML mediated a burst of reactive oxygen species and impeded mitochondrial activity and ATP reservoirs in microglia. We validated the age-dependent rise in CML levels in the sera and brains of humans. Finally, a microbiota-dependent increase in intestinal permeability in aged mice mediated the elevated levels of CML. This study adds insight into how specific features of microglia from aged mice are regulated by the gut microbiota.