Evidence map›Paper›PMID 37169935›Full record

ReviewJournal of neural transmission (Vienna, Austria : 1996)2023

The heterogeneity of Parkinson's disease.

Ullrich Wüllner, Per Borghammer, Chi-Un Choe, Ilona Csoti, Björn Falkenburger, Thomas Gasser, Paul Lingor, Peter Riederer

Abstract readReview
In one paragraph

Review in Journal of neural transmission (Vienna, Austria : 1996), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing 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

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

  1. Pooled it
  2. Article
  3. Review
  4. A qPCR-based approach targeting the microbial gene markerJournal of Parkinson's disease · 2026
    Article
  5. A novel rat model of body first subtype of Parkinson's disease.bioRxiv : the preprint server for biology · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

8 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

8 authors.

Ullrich WüllnerDepartment of Neurology, University Clinic Bonn and German Center for Neurodegenerative Diseases (DZNE), 53127, Bonn, Germany. wuellner@uni-bonn.de.ORCID http://orcid.org/0000-0002-3132-0790
Per BorghammerDepartment of Nuclear Medicine and PET, Aarhus University Hospital, Aarhus, Denmark.
Chi-Un ChoeDepartment of Neurology, Klinikum Itzehoe, Robert-Koch-Straße 2, 25524, Itzehoe, Germany.
Ilona CsotiFachklinik Für Parkinson, Gertrudis Klinik Biskirchen, Karl-Ferdinand-Broll-Straße 2-4, 35638, Leun-Biskirchen, Germany.
Björn FalkenburgerDepartment of Neurology, University Hospital Dresden, Fetscherstrasse 74, 01307, Dresden, Germany.
Thomas GasserDepartment of Neurology, Hertie-Institute for Clinical Brain Research, University of Tübingen and German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany.
Paul LingorDepartment of Neurology, School of Medicine, Klinikum Rechts Der Isar, Technical University of Munich, Munich, Germany.
Peter RiedererUniversity Hospital Wuerzburg, Clinic and Policlinic for Psychiatry, Psychosomatics and Psychotherapy, Margarete-Höppel-Platz 1, 97080, Würzburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The heterogeneity of Parkinson's disease (PD), i.e. the various clinical phenotypes, pathological findings, genetic predispositions and probably also the various implicated pathophysiological pathways pose a major challenge for future research projects and therapeutic trail design. We outline several pathophysiological concepts, pathways and mechanisms, including the presumed roles of α-synuclein misfolding and aggregation, Lewy bodies, oxidative stress, iron and melanin, deficient autophagy processes, insulin and incretin signaling, T-cell autoimmunity, the gut-brain axis and the evidence that microbial (viral) agents may induce molecular hallmarks of neurodegeneration. The hypothesis is discussed, whether PD might indeed be triggered by exogenous (infectious) agents in susceptible individuals upon entry via the olfactory bulb (brain first) or the gut (body-first), which would support the idea that disease mechanisms may change over time. The unresolved heterogeneity of PD may have contributed to the failure of past clinical trials, which attempted to slow the course of PD. We thus conclude that PD patients need personalized therapeutic approaches tailored to specific phenomenological and etiologic subtypes of disease.

Indexed as

Parkinson Diseasealpha-SynucleinBrainHumansLewy BodiesT-Lymphocytesalpha-SynucleinDisease mechanismInflammationParkinson’s diseasePathophysiologyPersonalized medicinePhenotypes

Identifiers

PMID37169935
PMCPMC10174621

What OpenQuestion holds

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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.