Evidence map›Paper›PMID 26886723›Full record

ArticleAntioxidants & redox signaling2016

18α-Glycyrrhetinic Acid Proteasome Activator Decelerates Aging and Alzheimer's Disease Progression in Caenorhabditis elegans and Neuronal Cultures.

Nikoletta Papaevgeniou, Marianthi Sakellari, Sweta Jha, Nektarios Tavernarakis, Carina I Holmberg, Efstathios S Gonos, Niki Chondrogianni

Open access · hybridAbstract read
In one paragraph

Article in Antioxidants & redox signaling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

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  20. Terpenoids as Potential Geroprotectors.Antioxidants (Basel, Switzerland) · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 5 countries.

Nikoletta Papaevgeniou1 Institute of Biology, Medicinal Chemistry and Biotechnology, National Hellenic Research Foundation , Athens, Greece .
Marianthi Sakellari1 Institute of Biology, Medicinal Chemistry and Biotechnology, National Hellenic Research Foundation , Athens, Greece .
Sweta Jha4 Translational Cancer Biology Program, Research Programs Unit, University of Helsinki , Helsinki, Finland .
Nektarios Tavernarakis5 Institute of Molecular Biology and Biotechnology , Foundation for Research and Technology-Hellas, Heraklion, Greece .
Carina I Holmberg4 Translational Cancer Biology Program, Research Programs Unit, University of Helsinki , Helsinki, Finland .
Efstathios S Gonos1 Institute of Biology, Medicinal Chemistry and Biotechnology, National Hellenic Research Foundation , Athens, Greece .
Niki Chondrogianni1 Institute of Biology, Medicinal Chemistry and Biotechnology, National Hellenic Research Foundation , Athens, Greece .
National Hellenic Research Foundation · GRÖrebro University · SEUniversity of Helsinki · FIUniversity of Crete · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsProteasomes 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.

resultsFeeding 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.

conclusionOur 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.

Indexed as

AgingAlzheimer DiseaseAmyloid beta-PeptidesAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell DeathCells, CulturedDisease ProgressionGlycyrrhetinic AcidLongevityNeuronsOxidation-ReductionPhenotypeProteasome Endopeptidase ComplexProtein Aggregation, Pathological18alpha-glycyrrhetinic acidAmyloid beta-PeptidesCaenorhabditis elegans ProteinsGlycyrrhetinic AcidProteasome Endopeptidase ComplexaggregationagingAlzheimer's diseaselifespan extensionproteasome activationproteostasis

Identifiers

PMID26886723
PMCPMC5124744
OpenAlexW2315885138

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.