Evidence map›Paper›PMID 32632204›Full record

ArticleMolecular psychiatry2021

Loss of function of the mitochondrial peptidase PITRM1 induces proteotoxic stress and Alzheimer's disease-like pathology in human cerebral organoids.

María José Pérez, Dina Ivanyuk, Vasiliki Panagiotakopoulou, Gabriele Di Napoli, Stefanie Kalb, Dario Brunetti, Rawaa Al-Shaana, Stephan A Kaeser, Sabine Anne-Kristin Fraschka, Mathias Jucker and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 2 pooled it
9.9field-weighted citation impact, top 1% 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

88 citing papers in PubMed, 2 syntheses or guidelines pooled it, 136 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Mitochondrial dysfunction in Alzheimer's disease: Guiding the path to targeted therapies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review

28 more citing papers are in PubMed but not listed here.

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

13 authors at 4 institutions in 3 countries.

María José Pérez *German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany.
Dina Ivanyuk *German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany.
Vasiliki PanagiotakopoulouGerman Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany.
Gabriele Di NapoliGerman Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany.
Stefanie KalbGerman Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany.
Dario BrunettiDepartment of Medical Biotechnology and Translational Medicine, University of Milan, Milan, Italy.
Rawaa Al-ShaanaGerman Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany.
Stephan A KaeserGerman Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany.
Sabine Anne-Kristin FraschkaDFG NGS Competence Center Tübingen, 72076, Tübingen, Germany.
Mathias JuckerGerman Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany.
Massimo ZevianiMRC-Mitochondrial Biology Unit, Cambridge, CB2 0XY, UK.
Carlo ViscomiMRC-Mitochondrial Biology Unit, Cambridge, CB2 0XY, UK.
Michela DeleidiGerman Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany. michela.deleidi@dzne.de.ORCID http://orcid.org/0000-0003-0357-0124
German Center for Neurodegenerative Diseases · DEMRC Mitochondrial Biology Unit · GBBernstein Center for Computational Neuroscience Tübingen · DEUniversity of Milan · IT

Funding

Medical Research Council MC_EX_MR/P007031/1Medical Research Council MC_UP_1002/1Medical Research Council MC_UU_00015/5MRF_ MRF-155-0001-S-MARTIMRF_ MRF-155-0002-RG-ZEVIAMRF_ MRF-155-0005-RG-ZEVI-C0784
6 · The paper itself

Abstract

Mutations in pitrilysin metallopeptidase 1 (PITRM1), a mitochondrial protease involved in mitochondrial precursor processing and degradation, result in a slow-progressing syndrome characterized by cerebellar ataxia, psychotic episodes, and obsessive behavior, as well as cognitive decline. To investigate the pathogenetic mechanisms of mitochondrial presequence processing, we employed cortical neurons and cerebral organoids generated from PITRM1-knockout human induced pluripotent stem cells (iPSCs). PITRM1 deficiency strongly induced mitochondrial unfolded protein response (UPR

Indexed as

Alzheimer DiseaseInduced Pluripotent Stem CellsAmyloid beta-PeptidesHumansMetalloendopeptidasesMitochondriaOrganoidsAmyloid beta-PeptidesMetalloendopeptidasesPITRM1 protein, human

Identifiers

PMID32632204
PMCPMC8758476
OpenAlexW3038196404

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.