Evidence map›Paper›PMID 30154511›Full record

Trial reportScientific reports2018

Self-report data as a tool for subtype identification in genetically-defined Parkinson's Disease.

Ashley R Winslow, Craig L Hyde, Jemma B Wilk, Nicholas Eriksson, Paul Cannon, Melissa R Miller, Warren D Hirst

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Genetic Modifiers of Parkinson's Disease: A Case-Control Study.Annals of clinical and translational neurology · 2025
    Observational
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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

7 authors at 4 institutions in 1 country.

Ashley R WinslowHuman Genetics and Computational Biomedicine, Pfizer Worldwide Research and Development, 1 Portland Street, Cambridge, MA, 02139, USA. awinslow@upenn.edu.ORCID 0000-0003-1265-5023
Craig L HydeEarly Clinical Development, Pfizer Worldwide Research and Development, 558 Eastern Point Rd., Groton, CT, 06340, USA.
Jemma B WilkHuman Genetics and Computational Biomedicine, Pfizer Worldwide Research and Development, 1 Portland Street, Cambridge, MA, 02139, USA.
Nicholas Eriksson23andMe Inc., 899W. Evelyn Avenue, Mountain View, CA, 94041, USA.
Paul Cannon23andMe Inc., 899W. Evelyn Avenue, Mountain View, CA, 94041, USA.
Melissa R MillerHuman Genetics and Computational Target Validation, Pfizer Worldwide Research and Development, 1 Portland Street, Cambirdge, MA, 02139, USA.
Warren D HirstNeuroscience, Pfizer Worldwide Research and Development, 1 Portland Street, Cambridge, MA, 02139, USA.
Pfizer (United States) · US23andMe (United States) · USBiogen (United States) · USTarget (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Through a targeted recruitment 23andMe has collected DNA and patient-reported symptoms from more than 10,000 subjects reporting a physician-verified diagnosis of PD. This study evaluated the potential of self-report, web-based questionnaires to rapidly assess disease natural history and symptomology in genetically-defined PD populations. While average age-at-diagnosis was significantly lower in GBA mutation carriers compared to idiopathic PD, or iPD (idiopathic PD, defined as no GBA mutations and no LRRK2 G2019S mutation), there were no significant differences in symptoms. Conversely, LRRK2 G2019S carrier status significantly associated with reporting of milder daily symptoms of lightheadedness and several differences were observed at a false discovery rate < 0.1, including increased reporting of changes in walking as an initial symptom of disease, decreased reporting of lightheadedness upon standing, and milder symptoms related to daily functioning. The subclinical differences in symptoms reported by LRRK2 G2019S carriers suggest differences in underlying pathophysiology and/or disease progression in LRRK2 carriers compared to iPD. Importantly, we confirm previous findings in PD genetic subsets where disease characteristics were ascertained through clinical exam. Overall, these data support the effective use of self-report and genetic data to rapidly analyze information from a large disease population or difficult to identify genetic subgroups.

Indexed as

Mutation, MissenseParkinson DiseaseSelf ReportActivities of Daily LivingAdultFemaleGlucosylceramidaseHumansLeucine-Rich Repeat Serine-Threonine Protein Kinase-2MaleMiddle AgedSurveys and QuestionnairesGBA protein, humanGlucosylceramidaseLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, human

Identifiers

PMID30154511
PMCPMC6113219
OpenAlexW2888594176

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.