Evidence map›Paper›PMID 39580573›Full record

ArticleCommunications biology2024

Modeling early phenotypes of Parkinson's disease by age-induced midbrain-striatum assembloids.

Kyriaki Barmpa, Claudia Saraiva, Diego Lopez-Pigozzi, Gemma Gomez-Giro, Elisa Gabassi, Sarah Spitz, Konstanze Brandauer, Juan E Rodriguez Gatica, Paul Antony, Graham Robertson and 11 more

Abstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Review
  2. Article
  3. Engineering brain organoids: from neurodevelopmental modeling to translational barriers.Journal of artificial organs : the official journal of the Japanese Society for Artificial Organs · 2026
    Review
  4. Parkinson's Disease Patient-Specific Striatum Organoids Show Hallmarks of Increased Inflammation.Movement disorders : official journal of the Movement Disorder Society · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. 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

21 authors.

Kyriaki BarmpaDevelopmental and Cellular Biology, Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg.
Claudia SaraivaDevelopmental and Cellular Biology, Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg.
Diego Lopez-PigozziDepartment of Physics and Astronomy "G. Galilei", University of Padua, Padua, Italy.ORCID 0000-0002-6178-5951
Gemma Gomez-GiroDevelopmental and Cellular Biology, Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg.
Elisa GabassiGenomics, Stem Cell & Regenerative Medicine Group and CMBI, Institute of Molecular Biology, University of Innsbruck, Innsbruck, Austria.ORCID 0000-0001-6053-503X
Sarah SpitzInstitute of Applied Synthetic Chemistry, Vienna University of Technology, Vienna, Austria.
Konstanze BrandauerInstitute of Applied Synthetic Chemistry, Vienna University of Technology, Vienna, Austria.
Juan E Rodriguez GaticaClausius Institute of Physical and Theoretical Chemistry, University of Bonn, Bonn, Germany.ORCID 0000-0003-4123-0104
Paul AntonyDevelopmental and Cellular Biology, Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg.ORCID 0000-0002-0450-9301
Graham RobertsonDevelopmental and Cellular Biology, Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg.
Rahman Sabahi-KavianiEindhoven University of Technology, Microsystems, Eindhoven, Netherlands.
Alessandro BellapiantaJohannes Kepler University Linz, Kepler University Hospital, University Clinic for Ophthalmology and Optometry, Linz, Austria.
Florentia PapastefanakiLaboratory of Cellular and Molecular Neurobiology-Stem Cells, Hellenic Pasteur Institute, Athens, Greece.
Regina LuttgeEindhoven University of Technology, Microsystems, Eindhoven, Netherlands.
Ulrich KubitscheckClausius Institute of Physical and Theoretical Chemistry, University of Bonn, Bonn, Germany.ORCID 0000-0003-3750-5355
Ahmad SaltiGenomics, Stem Cell & Regenerative Medicine Group and CMBI, Institute of Molecular Biology, University of Innsbruck, Innsbruck, Austria.ORCID 0000-0002-7678-0125
Peter ErtlInstitute of Applied Synthetic Chemistry, Vienna University of Technology, Vienna, Austria.
Mario BortolozziDepartment of Physics and Astronomy "G. Galilei", University of Padua, Padua, Italy.
Rebecca MatsasLaboratory of Cellular and Molecular Neurobiology-Stem Cells, Hellenic Pasteur Institute, Athens, Greece.ORCID 0000-0002-4027-348X
Frank EdenhoferGenomics, Stem Cell & Regenerative Medicine Group and CMBI, Institute of Molecular Biology, University of Innsbruck, Innsbruck, Austria.ORCID 0000-0002-6489-714X
Jens C SchwambornDevelopmental and Cellular Biology, Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Esch-sur-Alzette, Luxembourg. jens.schwamborn@uni.lu.ORCID 0000-0003-4496-0559

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) 459047646Deutsche Forschungsgemeinschaft (German Research Foundation) KU 2474/13-2EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020) 824070Fonds National de la Recherche Luxembourg (National Research Fund) C22/BM/17193204/MidStriPDFonds National de la Recherche Luxembourg (National Research Fund) NTER/FWF/19/14117540/PDage
6 · The paper itself

Abstract

Parkinson's disease, an aging-associated neurodegenerative disorder, is characterised by nigrostriatal pathway dysfunction caused by the gradual loss of dopaminergic neurons in the substantia nigra pars compacta of the midbrain. Human in vitro models are enabling the study of the dopaminergic neurons' loss, but not the dysregulation within the dopaminergic network in the nigrostriatal pathway. Additionally, these models do not incorporate aging characteristics which potentially contribute to the development of Parkinson's disease. Here we present a nigrostriatal pathway model based on midbrain-striatum assembloids with inducible aging. We show that these assembloids can develop characteristics of the nigrostriatal connectivity, with catecholamine release from the midbrain to the striatum and synapse formation between midbrain and striatal neurons. Moreover, Progerin-overexpressing assembloids acquire aging traits that lead to early neurodegenerative phenotypes. This model shall help to reveal the contribution of aging as well as nigrostriatal connectivity to the onset and progression of Parkinson's disease.

Indexed as

AgingMesencephalonParkinson DiseasePhenotypeAnimalsCorpus StriatumDopaminergic NeuronsHumansSubstantia Nigra

Identifiers

PMID39580573
PMCPMC11585662

What OpenQuestion holds

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Registered trials

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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.