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Projekt Druckansicht

Regulation der Wirkung von Antidepressiva durch Sphingomyelin- und Ceramid-kontrollierte Autophagie

Fachliche Zuordnung Biologische Psychiatrie
Anatomie und Physiologie
Förderung Förderung von 2013 bis 2024
Projektkennung Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 248884541
 
Erstellungsjahr 2024

Zusammenfassung der Projektergebnisse

In the present grant period we were able to identify a novel mechanism how major depressive disorder is induced. We demonstrated that major depressive disorder in humans, chronic unpredictable stress or glucocorticoid-mediated stress in mice results in an increase of ceramide in the blood plasma. Neutralization of ceramide in the blood plasma prevented or cured, respectively, major depressive disorder in mice. The increase of ceramide is mediated by neutral sphingomyelinase 2 (Smpd3). This is a completely novel mechanism to explain major depressive disorder. We identified targets of blood plasma ceramide in endothelial cells of the brain, i.e. phospholipase D and its product phosphatidic acid. Ceramide inhibits the function of phospholipase D and reduces phosphatidic acid. Since phosphatidic acid is much more polar than ceramide, it is able to diffuse into the brain and regulate functions in neurons and glia cells. We identified TrkB, induction of tyrosine-nitrosylation and most importantly the regulation of autophagy as targets of phosphatidic acid. We further confirmed the acid sphingomyelinase as target of antidepressants and applied this finding to the infection of cells and patients receiving antidepressants with SARS-CoV-2.

Projektbezogene Publikationen (Auswahl)

 
 

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