Evidence map›Paper›PMID 39095390›Full record

ArticleNature communications2024

Huntington's disease cellular phenotypes are rescued non-cell autonomously by healthy cells in mosaic telencephalic organoids.

Maura Galimberti, Maria R Nucera, Vittoria D Bocchi, Paola Conforti, Elena Vezzoli, Matteo Cereda, Camilla Maffezzini, Raffaele Iennaco, Andrea Scolz, Andrea Falqui and 10 more

Erratum issuedAbstract 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. An erratum has been issued. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
–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

17 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Towards AI-driven prediction ofJournal of Huntington's disease · 2026
    Article
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  6. Review
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  10. Exploring huntington's disease from a neurodevelopmental perspective.International journal of biological sciences · 2026
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors.

Maura GalimbertiLaboratory of Stem Cell Biology and Pharmacology of Neurodegenerative Diseases, Department of Biosciences, University of Milan, 20122, Milan, Italy.
Maria R NuceraLaboratory of Stem Cell Biology and Pharmacology of Neurodegenerative Diseases, Department of Biosciences, University of Milan, 20122, Milan, Italy.ORCID 0000-0001-8859-8884
Vittoria D BocchiLaboratory of Stem Cell Biology and Pharmacology of Neurodegenerative Diseases, Department of Biosciences, University of Milan, 20122, Milan, Italy.
Paola ConfortiLaboratory of Stem Cell Biology and Pharmacology of Neurodegenerative Diseases, Department of Biosciences, University of Milan, 20122, Milan, Italy.
Elena VezzoliLaboratory of Stem Cell Biology and Pharmacology of Neurodegenerative Diseases, Department of Biosciences, University of Milan, 20122, Milan, Italy.
Matteo CeredaLaboratory of Stem Cell Biology and Pharmacology of Neurodegenerative Diseases, Department of Biosciences, University of Milan, 20122, Milan, Italy.ORCID 0009-0008-5134-6390
Camilla MaffezziniLaboratory of Stem Cell Biology and Pharmacology of Neurodegenerative Diseases, Department of Biosciences, University of Milan, 20122, Milan, Italy.ORCID 0000-0002-0397-1609
Raffaele IennacoLaboratory of Stem Cell Biology and Pharmacology of Neurodegenerative Diseases, Department of Biosciences, University of Milan, 20122, Milan, Italy.
Andrea ScolzLaboratory of Stem Cell Biology and Pharmacology of Neurodegenerative Diseases, Department of Biosciences, University of Milan, 20122, Milan, Italy.
Andrea FalquiDepartment of Physics "Aldo Pontremoli", University of Milan, Via Celoria 16, 20133, Milan, Italy.ORCID 0000-0002-1476-7742
Chiara CordiglieriINGM, Istituto Nazionale Genetica Molecolare "Romeo ed Enrica Invernizzi", Milan, Italy.ORCID 0000-0002-2013-0043
Martina CremonaLaboratory of Stem Cell Biology and Pharmacology of Neurodegenerative Diseases, Department of Biosciences, University of Milan, 20122, Milan, Italy.
Ira Espuny-CamachoLaboratory of Stem Cell Biology and Pharmacology of Neurodegenerative Diseases, Department of Biosciences, University of Milan, 20122, Milan, Italy.ORCID 0000-0002-2356-2159
Andrea FaedoLaboratory of Stem Cell Biology and Pharmacology of Neurodegenerative Diseases, Department of Biosciences, University of Milan, 20122, Milan, Italy.
Dan P FelsenfeldCHDI Management/CHDI Foundation, New York, NY, USA.
Thomas F VogtCHDI Management/CHDI Foundation, New York, NY, USA.
Valeria RanzaniINGM, Istituto Nazionale Genetica Molecolare "Romeo ed Enrica Invernizzi", Milan, Italy.
Chiara ZuccatoLaboratory of Stem Cell Biology and Pharmacology of Neurodegenerative Diseases, Department of Biosciences, University of Milan, 20122, Milan, Italy.
Dario BesussoLaboratory of Stem Cell Biology and Pharmacology of Neurodegenerative Diseases, Department of Biosciences, University of Milan, 20122, Milan, Italy.
Elena CattaneoLaboratory of Stem Cell Biology and Pharmacology of Neurodegenerative Diseases, Department of Biosciences, University of Milan, 20122, Milan, Italy. elena.cattaneo@unimi.it.ORCID 0000-0002-0755-4917

Funding

CHDI Foundation (CHDI Foundation, Inc.) JSC A11103
6 · The paper itself

Abstract

Huntington's disease (HD) causes selective degeneration of striatal and cortical neurons, resulting in cell mosaicism of coexisting still functional and dysfunctional cells. The impact of non-cell autonomous mechanisms between these cellular states is poorly understood. Here we generated telencephalic organoids with healthy or HD cells, grown separately or as mosaics of the two genotypes. Single-cell RNA sequencing revealed neurodevelopmental abnormalities in the ventral fate acquisition of HD organoids, confirmed by cytoarchitectural and transcriptional defects leading to fewer GABAergic neurons, while dorsal populations showed milder phenotypes mainly in maturation trajectory. Healthy cells in mosaic organoids restored HD cell identity, trajectories, synaptic density, and communication pathways upon cell-cell contact, while showing no significant alterations when grown with HD cells. These findings highlight cell-type-specific alterations in HD and beneficial non-cell autonomous effects of healthy cells, emphasizing the therapeutic potential of modulating cell-cell communication in disease progression and treatment.

Indexed as

Huntington DiseaseOrganoidsPhenotypeTelencephalonAnimalsCell CommunicationGABAergic NeuronsHumansMiceMosaicismNeuronsSingle-Cell Analysis

Identifiers

PMID39095390
PMCPMC11297310

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.