Evidence map›Paper›PMID 37024503›Full record

ArticleNature communications2023

Genipin prevents alpha-synuclein aggregation and toxicity by affecting endocytosis, metabolism and lipid storage.

Rita Rosado-Ramos, Gonçalo M Poças, Daniela Marques, Alexandre Foito, David M Sevillano, Mafalda Lopes-da-Silva, Luís G Gonçalves, Regina Menezes, Marcel Ottens, Derek Stewart and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.0field-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

12 citing papers in PubMed, 23 citations in OpenAlex.

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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

17 authors at 6 institutions in 5 countries.

Rita Rosado-Ramos *iBET, Instituto de Biologia Experimental e Tecnológica, Oeiras, Portugal.
Gonçalo M Poças *Instituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa (ITQB NOVA), Oeiras, Portugal.ORCID 0000-0001-8774-1618
Daniela MarquesiNOVA4Health, NOVA Medical School Faculdade de Ciências Médicas, NMS FCM, Universidade Nova de Lisboa, Lisboa, Portugal.
Alexandre FoitoEnvironmental and Biochemical Sciences, The James Hutton Institute, DD2 5DA, Dundee, Scotland.
David M SevillanoDepartment of Biotechnology, Delft University of Technology, Delft, Netherlands.
Mafalda Lopes-da-SilvaiNOVA4Health, NOVA Medical School Faculdade de Ciências Médicas, NMS FCM, Universidade Nova de Lisboa, Lisboa, Portugal.
Luís G GonçalvesInstituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa (ITQB NOVA), Oeiras, Portugal.
Regina MenezesiBET, Instituto de Biologia Experimental e Tecnológica, Oeiras, Portugal.
Marcel OttensDepartment of Biotechnology, Delft University of Technology, Delft, Netherlands.
Derek StewartEnvironmental and Biochemical Sciences, The James Hutton Institute, DD2 5DA, Dundee, Scotland.
Alain Ibáñez de OpakuaGerman Center for Neurodegenerative Diseases (DZNE), 37075, Göttingen, Germany.
Markus ZweckstetterGerman Center for Neurodegenerative Diseases (DZNE), 37075, Göttingen, Germany.ORCID 0000-0002-2536-6581
Miguel C SeabraiNOVA4Health, NOVA Medical School Faculdade de Ciências Médicas, NMS FCM, Universidade Nova de Lisboa, Lisboa, Portugal.
César S MendesiNOVA4Health, NOVA Medical School Faculdade de Ciências Médicas, NMS FCM, Universidade Nova de Lisboa, Lisboa, Portugal.
Tiago Fleming OuteiroGerman Center for Neurodegenerative Diseases (DZNE), 37075, Göttingen, Germany.
Pedro M DomingosInstituto de Tecnologia Química e Biológica António Xavier, Universidade Nova de Lisboa (ITQB NOVA), Oeiras, Portugal.ORCID 0000-0003-4523-5631
Cláudia N SantosiBET, Instituto de Biologia Experimental e Tecnológica, Oeiras, Portugal. claudia.nunes.santos@nms.unl.pt.ORCID 0000-0002-5809-1924
Universidade Nova de Lisboa · PTGerman Center for Neurodegenerative Diseases · DEDelft University of Technology · NLInstituto de Biologia Experimental e Tecnológica · PTJames Hutton Institute · GBNova Medical (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's Disease (PD) is a common neurodegenerative disorder affecting millions of people worldwide for which there are only symptomatic therapies. Small molecules able to target key pathological processes in PD have emerged as interesting options for modifying disease progression. We have previously shown that a (poly)phenol-enriched fraction (PEF) of Corema album L. leaf extract modulates central events in PD pathogenesis, namely α-synuclein (αSyn) toxicity, aggregation and clearance. PEF was now subjected to a bio-guided fractionation with the aim of identifying the critical bioactive compound. We identified genipin, an iridoid, which relieves αSyn toxicity and aggregation. Furthermore, genipin promotes metabolic alterations and modulates lipid storage and endocytosis. Importantly, genipin was able to prevent the motor deficits caused by the overexpression of αSyn in a Drosophila melanogaster model of PD. These findings widens the possibility for the exploitation of genipin for PD therapeutics.

Indexed as

alpha-SynucleinParkinson DiseaseAnimalsDrosophila melanogasterIridoidsLipidsPhenolsalpha-SynucleingenipinIridoidsLipidsPhenols

Identifiers

PMID37024503
PMCPMC10079842
OpenAlexW4362666335

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.