Evidence map›Paper›PMID 32190419›Full record

ArticleNeurology. Clinical practice2020

Serum FGF-21, GDF-15, and blood mtDNA copy number are not biomarkers of Parkinson disease.

Ryan L Davis, Siew L Wong, Phillippa J Carling, Thomas Payne, Carolyn M Sue, Oliver Bandmann

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurology. Clinical practice, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 4 pooled it
3.7field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 4 syntheses or guidelines pooled it, 32 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  8. Article
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  10. Article
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  12. Article
  13. Parkinson's disease therapy: what lies ahead?Journal of neural transmission (Vienna, Austria : 1996) · 2023
    Review
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  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Genotype-driven therapeutic developments in Parkinson's disease.Molecular medicine (Cambridge, Mass.) · 2021
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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

6 authors at 3 institutions in 2 countries.

Ryan L DavisDepartment of Neurogenetics (RLD, CMS), University of Sydney, Kolling Institute and Royal North Shore Hospital, St Leonards, Sydney, New South Wales, Australia; Department of Neuroscience (SLW, PJC, TP, OB), Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, United Kingdom; and Department of Neurology (CMS), Royal North Shore Hospital, Northern Sydney Local Health District, St Leonards, Sydney, New South Wales, Australia.
Siew L WongDepartment of Neurogenetics (RLD, CMS), University of Sydney, Kolling Institute and Royal North Shore Hospital, St Leonards, Sydney, New South Wales, Australia; Department of Neuroscience (SLW, PJC, TP, OB), Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, United Kingdom; and Department of Neurology (CMS), Royal North Shore Hospital, Northern Sydney Local Health District, St Leonards, Sydney, New South Wales, Australia.
Phillippa J CarlingDepartment of Neurogenetics (RLD, CMS), University of Sydney, Kolling Institute and Royal North Shore Hospital, St Leonards, Sydney, New South Wales, Australia; Department of Neuroscience (SLW, PJC, TP, OB), Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, United Kingdom; and Department of Neurology (CMS), Royal North Shore Hospital, Northern Sydney Local Health District, St Leonards, Sydney, New South Wales, Australia.
Thomas PayneDepartment of Neurogenetics (RLD, CMS), University of Sydney, Kolling Institute and Royal North Shore Hospital, St Leonards, Sydney, New South Wales, Australia; Department of Neuroscience (SLW, PJC, TP, OB), Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, United Kingdom; and Department of Neurology (CMS), Royal North Shore Hospital, Northern Sydney Local Health District, St Leonards, Sydney, New South Wales, Australia.
Carolyn M SueDepartment of Neurogenetics (RLD, CMS), University of Sydney, Kolling Institute and Royal North Shore Hospital, St Leonards, Sydney, New South Wales, Australia; Department of Neuroscience (SLW, PJC, TP, OB), Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, United Kingdom; and Department of Neurology (CMS), Royal North Shore Hospital, Northern Sydney Local Health District, St Leonards, Sydney, New South Wales, Australia.
Oliver BandmannDepartment of Neurogenetics (RLD, CMS), University of Sydney, Kolling Institute and Royal North Shore Hospital, St Leonards, Sydney, New South Wales, Australia; Department of Neuroscience (SLW, PJC, TP, OB), Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, United Kingdom; and Department of Neurology (CMS), Royal North Shore Hospital, Northern Sydney Local Health District, St Leonards, Sydney, New South Wales, Australia.
University of Sheffield · GBRoyal North Shore Hospital · AUUniversity of Sydney · AU

Funding

Medical Research Council MR/R011354/1Parkinson's UK G-1202
6 · The paper itself

Abstract

backgroundStrong evidence of mitochondrial dysfunction exists for both familial and sporadic Parkinson disease (PD). A simple test, reliably identifying mitochondrial dysfunction, could be important for future stratified medicine trials in PD. We previously undertook a comparison of serum biomarkers in classic mitochondrial diseases and established that serum growth differentiation factor 15 (GDF-15) outperforms fibroblast growth factor 21 (FGF-21) when distinguishing patients with mitochondrial diseases from healthy controls. This study aimed to systematically assess serum FGF-21 and GDF-15, together with mitochondrial DNA (mtDNA) copy number levels in peripheral blood cells from patients with PD and healthy controls, to determine whether these measures could act as a biomarker of PD.

methodsOne hundred twenty-one patients with PD and 103 age-matched healthy controls were recruited from a single center. Serum FGF-21 and GDF-15, along with blood mtDNA copy number, were quantified using established assays.

resultsThere were no meaningful differences identified for any of the measures when comparing patients with PD with healthy controls. This highlights a lack of diagnostic sensitivity that is incompatible with these measures being used as biomarkers for PD.

conclusionIn this study, serum FGF-21, serum GDF-15, and blood mtDNA levels were similar in patients with PD and healthy controls and therefore unlikely to be satisfactory indicators of mitochondrial dysfunction in patients with PD. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that serum FGF-21, serum GDF-15, and blood mtDNA copy number levels do not distinguish patients with PD from healthy controls. There was no diagnostic uncertainty between patients with PD and healthy controls.

Identifiers

PMID32190419
PMCPMC7057070
OpenAlexW2969646180

What OpenQuestion holds

Textmetadata
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.