Evidence mapPaperPMID 39231983Full record

ArticleNature communications2024

Cannabidiol ameliorates mitochondrial disease via PPARγ activation in preclinical models.

Emma Puighermanal, Marta Luna-Sánchez, Alejandro Gella, Gunter van der Walt, Andrea Urpi, María Royo, Paula Tena-Morraja, Isabella Appiah, Maria Helena de Donato, Fabien Menardy and 13 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
field-weighted citation impact
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

18 citing papers in PubMed.

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  18. Disease models of Leigh syndrome: From yeast to organoids.Journal of inherited metabolic disease · 2024
    Review
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

23 authors.

Emma PuighermanalInstitut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra, Spain. emma.puighermanal@uab.cat.ORCID 0000-0003-4271-9104
Marta Luna-SánchezInstitut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra, Spain.
Alejandro GellaInstitut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra, Spain.ORCID 0000-0002-3983-1392
Gunter van der WaltInstitut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra, Spain.
Andrea UrpiInstitut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra, Spain.
María RoyoInstitute of Neuroscience, CSIC-UMH, San Juan de Alicante, Spain.
Paula Tena-MorrajaCelltec-UB, Departament de Biologia Cel·lular, Fisiologia i Immunologia, Institut de Neurociències, Universitat de Barcelona, Barcelona, Spain.ORCID 0000-0002-7617-3392
Isabella AppiahInstitut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra, Spain.
Maria Helena de DonatoInstitut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra, Spain.ORCID 0009-0002-3602-3848
Fabien MenardyInstitut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra, Spain.
Patrizia BianchiInstitut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra, Spain.
Anna Esteve-CodinaCentro Nacional de Análisis Genómico (CNAG), Barcelona, Spain.ORCID 0000-0003-0361-2873
Laura Rodríguez-PascauMinoryx Therapeutics SL, Barcelona, Spain.ORCID 0000-0001-5631-1172
Cristina VergaraMinoryx Therapeutics BE SA, Gosselies, Charleroi, Belgium.ORCID 0000-0002-4263-1340
Mercè Gómez-PallarèsInstitut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra, Spain.
Giovanni MarsicanoInserm Université de Bordeaux, U1215 Neurocentre Magendie, Bordeaux, France.ORCID 0000-0003-3804-1951
Luigi BellocchioInserm Université de Bordeaux, U1215 Neurocentre Magendie, Bordeaux, France.
Marc MartinellMinoryx Therapeutics SL, Barcelona, Spain.
Elisenda SanzInstitut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra, Spain.ORCID 0000-0002-7932-8556
Sandra JuradoInstitute of Neuroscience, CSIC-UMH, San Juan de Alicante, Spain.ORCID 0000-0001-9864-9307
Francesc Xavier SorianoCelltec-UB, Departament de Biologia Cel·lular, Fisiologia i Immunologia, Institut de Neurociències, Universitat de Barcelona, Barcelona, Spain.ORCID 0000-0003-1678-7162
Pilar PizcuetaMinoryx Therapeutics SL, Barcelona, Spain.ORCID 0000-0002-8444-8886
Albert QuintanaInstitut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra, Spain. albert.quintana@uab.cat.ORCID 0000-0003-1674-7160

Funding

EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) ERC-2014-StG-638106EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 Marie Skłodowska-Curie Actions (H2020 Excellent Science - Marie Skłodowska-Curie Actions) H2020-MSCA-COFUND-2014-665919EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 Marie Skłodowska-Curie Actions (H2020 Excellent Science - Marie Skłodowska-Curie Actions) H2020-MSCA-IF-2014-658352EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 Marie Skłodowska-Curie Actions (H2020 Excellent Science - Marie Skłodowska-Curie Actions) H2020-MSCA-IF-2020-101030783,"la Caixa" Foundation (Caixa Foundation) LCF/PR/HR20/52400018.
6 · The paper itself

Abstract

Mutations in mitochondrial energy-producing genes lead to a heterogeneous group of untreatable disorders known as primary mitochondrial diseases (MD). Leigh syndrome (LS) is the most common pediatric MD and is characterized by progressive neuromuscular affectation and premature death. Here, we show that daily cannabidiol (CBD) administration significantly extends lifespan and ameliorates pathology in two LS mouse models, and improves cellular function in fibroblasts from LS patients. CBD delays motor decline and neurodegenerative signs, improves social deficits and breathing abnormalities, decreases thermally induced seizures, and improves neuropathology in affected brain regions. Mechanistically, we identify peroxisome proliferator-activated receptor gamma (PPARγ) as a key nuclear receptor mediating CBD's beneficial effects, while also providing proof of dysregulated PPARγ expression and activity as a common feature in both mouse neurons and fibroblasts from LS patients. Taken together, our results provide the first evidence for CBD as a potential treatment for LS.

Indexed as

CannabidiolMitochondrial DiseasesPPAR gammaAnimalsBrainDisease Models, AnimalFemaleFibroblastsHumansLeigh DiseaseMaleMiceMice, Inbred C57BLMitochondriaNeuronsCannabidiolPPAR gamma

Identifiers

PMID39231983
PMCPMC11375224

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.