Evidence map›Paper›PMID 38684731›Full record

ArticleNature communications2024

Mitochondrial complex I deficiency stratifies idiopathic Parkinson's disease.

Irene H Flønes, Lilah Toker, Dagny Ann Sandnes, Martina Castelli, Sepideh Mostafavi, Njål Lura, Omnia Shadad, Erika Fernandez-Vizarra, Cèlia Painous, Alexandra Pérez-Soriano and 7 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 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

17 authors.

Irene H FlønesNeuro-SysMed, Department of Neurology, Haukeland University Hospital, 5021, Bergen, Norway.
Lilah TokerNeuro-SysMed, Department of Neurology, Haukeland University Hospital, 5021, Bergen, Norway.ORCID http://orcid.org/0000-0002-6514-561X
Dagny Ann SandnesNeuro-SysMed, Department of Neurology, Haukeland University Hospital, 5021, Bergen, Norway.
Martina CastelliNeuro-SysMed, Department of Neurology, Haukeland University Hospital, 5021, Bergen, Norway.
Sepideh MostafaviNeuro-SysMed, Department of Neurology, Haukeland University Hospital, 5021, Bergen, Norway.
Njål LuraMohn Medical Imaging and Visualization Centre, Department of Radiology, Haukeland University Hospital, Bergen, Norway.
Omnia ShadadNeuro-SysMed, Department of Neurology, Haukeland University Hospital, 5021, Bergen, Norway.
Erika Fernandez-VizarraMRC-Mitochondrial Biology Unit, University of Cambridge, Hills Road, Cambridge, CB2 0XY, UK.ORCID http://orcid.org/0000-0002-2469-142X
Cèlia PainousParkinson's disease & Movement Disorders Unit, Neurology Service, Hospital Clínic I Universitari de Barcelona; IDIBAPS, CIBERNED (CB06/05/0018-ISCIII), ERN-RND, Institut Clínic de Neurociències (Maria de Maeztu excellence centre), Universitat de Barcelona, Barcelona, Catalonia, Spain.
Alexandra Pérez-SorianoParkinson's disease & Movement Disorders Unit, Neurology Service, Hospital Clínic I Universitari de Barcelona; IDIBAPS, CIBERNED (CB06/05/0018-ISCIII), ERN-RND, Institut Clínic de Neurociències (Maria de Maeztu excellence centre), Universitat de Barcelona, Barcelona, Catalonia, Spain.
Yaroslau ComptaParkinson's disease & Movement Disorders Unit, Neurology Service, Hospital Clínic I Universitari de Barcelona; IDIBAPS, CIBERNED (CB06/05/0018-ISCIII), ERN-RND, Institut Clínic de Neurociències (Maria de Maeztu excellence centre), Universitat de Barcelona, Barcelona, Catalonia, Spain.
Laura Molina-PorcelAlzheimer's disease and other cognitive disorders unit. Neurology Service, Hospital Clínic, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Barcelona, Spain.ORCID http://orcid.org/0000-0003-4068-8578
Guido AlvesThe Norwegian Centre for Movement Disorders and Department of Neurology, Stavanger University Hospital, Pb 8100, 4068, Stavanger, Norway.ORCID http://orcid.org/0000-0003-0630-2870
Ole-Bjørn TysnesNeuro-SysMed, Department of Neurology, Haukeland University Hospital, 5021, Bergen, Norway.ORCID http://orcid.org/0000-0002-7230-6426
Christian DölleNeuro-SysMed, Department of Neurology, Haukeland University Hospital, 5021, Bergen, Norway.ORCID http://orcid.org/0000-0003-2427-8130
Gonzalo S NidoNeuro-SysMed, Department of Neurology, Haukeland University Hospital, 5021, Bergen, Norway.ORCID http://orcid.org/0000-0002-1766-4108
Charalampos TzoulisNeuro-SysMed, Department of Neurology, Haukeland University Hospital, 5021, Bergen, Norway. charalampos.tzoulis@uib.no.ORCID http://orcid.org/0000-0003-0341-5191

Funding

Bergens Forskningsstiftelse (Bergen Research Foundation) BFS2017REK05
6 · The paper itself

Abstract

Idiopathic Parkinson's disease (iPD) is believed to have a heterogeneous pathophysiology, but molecular disease subtypes have not been identified. Here, we show that iPD can be stratified according to the severity of neuronal respiratory complex I (CI) deficiency, and identify two emerging disease subtypes with distinct molecular and clinical profiles. The CI deficient (CI-PD) subtype accounts for approximately a fourth of all cases, and is characterized by anatomically widespread neuronal CI deficiency, a distinct cell type-specific gene expression profile, increased load of neuronal mtDNA deletions, and a predilection for non-tremor dominant motor phenotypes. In contrast, the non-CI deficient (nCI-PD) subtype exhibits no evidence of mitochondrial impairment outside the dopaminergic substantia nigra and has a predilection for a tremor dominant phenotype. These findings constitute a step towards resolving the biological heterogeneity of iPD with implications for both mechanistic understanding and treatment strategies.

Indexed as

DNA, MitochondrialElectron Transport Complex IMitochondriaMitochondrial DiseasesParkinson DiseaseAgedFemaleHumansMaleMiddle AgedNeuronsPhenotypeSubstantia NigraDNA, MitochondrialElectron Transport Complex I

Identifiers

PMID38684731
PMCPMC11059185

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.