Dokument: Abl depletion via autophagy mediates the beneficial effects of quercetin against Alzheimer pathology across species

Titel:Abl depletion via autophagy mediates the beneficial effects of quercetin against Alzheimer pathology across species
URL für Lesezeichen:https://docserv.uni-duesseldorf.de/servlets/DocumentServlet?id=67536
URN (NBN):urn:nbn:de:hbz:061-20241115-112149-0
Kollektion:Publikationen
Sprache:Englisch
Dokumententyp:Wissenschaftliche Texte » Artikel, Aufsatz
Medientyp:Text
Autoren: Schiavi, Alfonso [Autor]
Cirotti, Claudia [Autor]
Gerber, Lora-Sophie [Autor]
Lauro, Giulia Di [Autor]
Maglioni, Silvia [Autor]
Tanaka Shibao, Priscila Yumi [Autor]
Montresor, Sabrina [Autor]
Kirstein, Janine [Autor]
Petzsch, Patrick [Autor]
Köhrer, Karl [Autor]
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Dateien vom 15.11.2024 / geändert 15.11.2024
Beschreibung:Alzheimer’s disease is the most common age-associated neurodegenerative disorder and the most frequent form of dementia in our society. Aging is a complex biological process concurrently shaped by genetic, dietary and environmental factors and natural compounds are emerging for their beneficial effects against age-related disorders. Besides their antioxidant activity often described in simple model organisms, the molecular mechanisms underlying the beneficial effects of different dietary compounds remain however largely unknown. In the present study, we exploit the nematode Caenorhabditis elegans as a widely established model for aging studies, to test the effects of different natural compounds in vivo and focused on mechanistic aspects of one of them, quercetin, using complementary systems and assays. We show that quercetin has evolutionarily conserved beneficial effects against Alzheimer’s disease (AD) pathology: it prevents Amyloid beta (Aβ)-induced detrimental effects in different C. elegans AD models and it reduces Aβ-secretion in mammalian cells. Mechanistically, we found that the beneficial effects of quercetin are mediated by autophagy-dependent reduced expression of Abl tyrosine kinase. In turn, autophagy is required upon Abl suppression to mediate quercetin’s protective effects against Aβ toxicity. Our data support the power of C. elegans as an in vivo model to investigate therapeutic options for AD.
Rechtliche Vermerke:Originalveröffentlichung:
Schiavi, A., Cirotti, C., Gerber, L.-S., Di Lauro, G., Maglioni, S., Shibao, P. Y. T., Montresor, S., Kirstein, J., Petzsch, P., Köhrer, K., Schins, R. P. F., Wahle, T., Barilà, D., & Ventura, N. (2023). Abl depletion via autophagy mediates the beneficial effects of quercetin against Alzheimer pathology across species. Cell Death Discovery, 9, Article 376. https://doi.org/10.1038/s41420-023-01592-x
Lizenz:Creative Commons Lizenzvertrag
Dieses Werk ist lizenziert unter einer Creative Commons Namensnennung 4.0 International Lizenz
Fachbereich / Einrichtung:Mathematisch- Naturwissenschaftliche Fakultät
Medizinische Fakultät
Dokument erstellt am:15.11.2024
Dateien geändert am:15.11.2024
english
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