Εξειδίκευση τύπου :	Άρθρο σε επιστημονικό περιοδικό
Τίτλος:	18α-Glycyrrhetinic acid proteasome activator decelerates aging and Alzheimer's disease progression in caenorhabditis elegans and neuronal cultures
Δημιουργός/Συγγραφέας:	Papaevgeniou N. Sakellari M. Jha S. Tavernarakis N. Holmberg C.I. [EL] Γκόνος, Ευστάθιος[EN] Gonos, Efstathios S. [EL] Χονδρογιάννη, Νίκη[EN] Chondrogianni, Niki
Εκδότης:	Mary Ann Liebert Inc.
Ημερομηνία:	2016
Γλώσσα:	Αγγλικά
ISSN:	1523-0864
DOI:	10.1089/ars.2015.6494
Άλλο:	PubMed ID: 26886723
Περίληψη:	Proteasomes are constituents of the cellular proteolytic networks that maintain protein homeostasis through regulated proteolysis of normal and abnormal (in any way) proteins. Genetically mediated proteasome activation in multicellular organisms has been shown to promote longevity and to exert protein antiaggregation activity. In this study, we investigate whether compound-mediated proteasome activation is feasible in a multicellular organism and we dissect the effects of such approach in aging and Alzheimer's disease (AD) progression. Results: Feeding of wild-type Caenorhabditis elegans with 18α-glycyrrhetinic acid (18α-GA; a previously shown proteasome activator in cell culture) results in enhanced levels of proteasome activities that lead to a skinhead-1- and proteasome activation-dependent life span extension. The elevated proteasome function confers lower paralysis rates in various AD nematode models accompanied by decreased Aβ deposits, thus ultimately decelerating the progression of AD phenotype. More importantly, similar positive results are also delivered when human and murine cells of nervous origin are subjected to 18α-GA treatment. Innovation: This is the first report of the use of 18α-GA, a diet-derived compound as prolongevity and antiaggregation factor in the context of a multicellular organism. Conclusion: Our results suggest that proteasome activation with downstream positive outcomes on aging and AD, an aggregation-related disease, is feasible in a nongenetic manipulation manner in a multicellular organism. Moreover, they unveil the need for identification of antiaging and antiamyloidogenic compounds among the nutrients found in our normal diet. Antioxid. Redox Signal. 25, 855-869.
Τίτλος πηγής δημοσίευσης:	Antioxidants and Redox Signaling
Τόμος/Κεφάλαιο:	25
Τεύχος:	16
Σελίδες:	855-869
Θεματική Κατηγορία:	[EL] Βιολογία (Γενικά)[EN] Biology (General)
Λέξεις-Κλειδιά:	aggregation aging Alzheimers disease lifespan extension proteasome activation proteostasis
Αξιολόγηση από ομότιμους (peer reviewed):	Ναι
Κάτοχος πνευματικών δικαιωμάτων:	© 2016, Mary Ann Liebert, Inc. 2016.
Όροι και προϋποθέσεις δικαιωμάτων:	All Open Access, Bronze, Green
Σημειώσεις:	266486 NU-AGE; QALHS AP:10479/3.7.12 MIS380228; European Commission, EC; European Cooperation in Science and Technology, COST: BM1307, GENiE BM1408; Academy of Finland: 259797; National Health Research Institutes, NHRI; European Social Fund, ESF. This work was funded by two Research Funding Programs: Thales GenAge [QALHS AP:10479/3.7.12 MIS380228] (to E.S.G. and N.C.) and MAESTRO (to N.C.) cofinanced by the European Union (European Social Fund) and Greek national funds through the Operational Program, Education and Lifelong Learning, of the National Strategic Reference Framework (NSRF), a European Union (266486 NU-AGE) grant (to E.S.G.), an IKYDA 2012 fellowship, an Empirikion Foundation Scientific Project and a Scientific Project funded by John S. Latsis Public Benefit Foundation (to N.C.), and by the Academy of Finland (259797 to C.I.H.). The present publication is supported by the COST Actions PROTEOSTASIS BM1307 and GENiE BM1408, supported by COST (European Cooperation in Science and Technology).
Εμφανίζεται στις συλλογές:	Ινστιτούτο Χημικής Βιολογίας - Επιστημονικό έργο