Evidence map›Paper›PMID 33002040›Full record

SynthesisPloS one2020

Meta-analysis of whole-exome sequencing data from two independent cohorts finds no evidence for rare variant enrichment in Parkinson disease associated loci.

Johannes Jernqvist Gaare, Gonzalo Nido, Christian Dölle, Paweł Sztromwasser, Guido Alves, Ole-Bjørn Tysnes, Kristoffer Haugarvoll, Charalampos Tzoulis

Abstract readMeta-Analysis
In one paragraph

Synthesis in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

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

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. 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

8 authors.

Johannes Jernqvist GaareDepartment of Neurology, Haukeland University Hospital, Bergen, Norway.
Gonzalo NidoDepartment of Neurology, Haukeland University Hospital, Bergen, Norway.ORCID 0000-0002-1766-4108
Christian DölleDepartment of Neurology, Haukeland University Hospital, Bergen, Norway.ORCID 0000-0003-2427-8130
Paweł SztromwasserDepartment of Clinical Science, University of Bergen, Bergen, Norway.ORCID 0000-0002-0661-8800
Guido AlvesThe Norwegian Centre for Movement Disorders and Department of Neurology, Stavanger University Hospital, Stavanger, Norway.
Ole-Bjørn TysnesDepartment of Neurology, Haukeland University Hospital, Bergen, Norway.
Kristoffer HaugarvollDepartment of Neurology, Haukeland University Hospital, Bergen, Norway.
Charalampos TzoulisDepartment of Neurology, Haukeland University Hospital, Bergen, Norway.ORCID 0000-0003-0341-5191

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson disease (PD) is a complex neurodegenerative disorder influenced by both environmental and genetic factors. While genome wide association studies have identified several susceptibility loci, many causal variants and genes underlying these associations remain undetermined. Identifying these is essential in order to gain mechanistic insight and identify biological pathways that may be targeted therapeutically. We hypothesized that gene-based enrichment of rare mutations is likely to be found within susceptibility loci for PD and may help identify causal genes. Whole-exome sequencing data from two independent cohorts were analyzed in tandem and by meta-analysis and a third cohort genotyped using the NeuroX-array was used for replication analysis. We employed collapsing methods (burden and the sequence kernel association test) to detect gene-based enrichment of rare, protein-altering variation within established PD susceptibility loci. Our analyses showed trends for three genes (GALC, PARP9 and SEC23IP), but none of these survived multiple testing correction. Our findings provide no evidence of rare mutation enrichment in genes within PD-associated loci, in our datasets. While not excluding that rare mutations in these genes may influence the risk of idiopathic PD, our results suggest that, if such effects exist, much larger sequencing datasets will be required for their detection.

Indexed as

ExomePolymorphism, Single NucleotideGalactosylceramidaseGenetic Predisposition to DiseaseNeoplasm ProteinsParkinson DiseasePoly(ADP-ribose) PolymerasesRNA-Binding ProteinsGalactosylceramidaseNeoplasm ProteinsPARP9 protein, humanPoly(ADP-ribose) PolymerasesRNA-Binding ProteinsSEC23IP protein, human

Identifiers

PMID33002040
PMCPMC7529297

What Socratic 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 Socratic graph.