Evidence map›Paper›PMID 35725575›Full record

ArticleNPJ Parkinson's disease2022

Cognition as a mediator for gait and balance impairments in GBA-related Parkinson's disease.

Rosie Morris, Douglas N Martini, Katrina Ramsey, Valerie E Kelly, Katrijn Smulders, Amie Hiller, Kathryn A Chung, Shu-Ching Hu, Cyrus P Zabetian, Kathleen L Poston and 7 more

Registry-linked trialOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in NPJ Parkinson's disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01720810 (Pacific Northwest Udall Center), which is not on this map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 23% 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.

NCT01720810 unknown statusnot on this map

Pacific Northwest Udall Center (PANUC) Clinical Core

TypeobservationalSponsorUniversity of WashingtonRan2010 to 2025Enrolled2,000ConditionsParkinson Disease, Cognitive Impairment
3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. Article
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  5. Review
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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

17 authors at 7 institutions in 3 countries.

Rosie MorrisDepartment of Neurology, Oregon Health and Science University, Portland, OR, USA.ORCID http://orcid.org/0000-0002-0290-6688
Douglas N MartiniDepartment of Neurology, Oregon Health and Science University, Portland, OR, USA.
Katrina RamseySchool of Public Health, Oregon Health and Science University, Portland, OR, USA.
Valerie E KellyDepartment of Rehabilitation Medicine, University of Washington School of Medicine, Seattle, WA, USA.
Katrijn SmuldersSint Maartenskliniek Research Department, Nijmegen, The Netherlands.
Amie HillerDepartment of Neurology, Oregon Health and Science University, Portland, OR, USA.
Kathryn A ChungDepartment of Neurology, Oregon Health and Science University, Portland, OR, USA.
Shu-Ching HuDepartment of Neurology, University of Washington School of Medicine, Seattle, WA, USA.
Cyrus P ZabetianDepartment of Neurology, University of Washington School of Medicine, Seattle, WA, USA.ORCID http://orcid.org/0000-0002-7739-4306
Kathleen L PostonDepartment of Neurology and Neurological Sciences, Stanford School of Medicine, Palo Alto, CA, USA.ORCID http://orcid.org/0000-0003-3424-7143
Ignacio F MataDepartment of Neurology, University of Washington School of Medicine, Seattle, WA, USA.ORCID http://orcid.org/0000-0003-1198-0633
Karen L EdwardsDepartment of Epidemiology and Biostatistics, University of California, Irvine, CA, USA.
Jodi LapidusSchool of Public Health, Oregon Health and Science University, Portland, OR, USA.
Brenna CholertonDepartment of Pathology, Stanford University School of Medicine, Palo Alto, CA, USA.ORCID http://orcid.org/0000-0002-2139-987X
Thomas J MontineDepartment of Pathology, Stanford University School of Medicine, Palo Alto, CA, USA.
Joseph F QuinnDepartment of Neurology, Oregon Health and Science University, Portland, OR, USA.
Fay HorakDepartment of Neurology, Oregon Health and Science University, Portland, OR, USA. horakf@ohsu.edu.
Oregon Health & Science University · USUniversity of Washington · USStanford University · USCleveland Clinic · USSint Maartenskliniek · NLStanford Medicine · USUniversity of California, Irvine · US

Funding

Oregon Clinical and Translational Research Institute - The National COVID Cohort Collaborative (N3C)UL1TR002369 · NCATS · OREGON HEALTH & SCIENCE UNIVERSITY · PI Cynthia D Morris, Christopher G. Slatore · 2017 to 2026
$78.4M
Udall Center Director's meeting poster awardP50NS062684 · NINDS · UNIVERSITY OF WASHINGTON · PI MONTINE, THOMAS J · 2009 to 2020
$18.3M
CSRD VA I01 CX001702NCATS NIH HHS UL1 TR002369NINDS NIH HHS P50 NS062684
6 · The paper itself

Abstract

The extent to which the heterogeneity of gait and balance problems in PD may be explained by genetic variation is unknown. Variants in the glucocerebrosidase (GBA) gene are the strongest known genetic risk factor for PD and are associated with greater motor and cognitive severity. However, the impact of GBA variants on comprehensive measures of gait and balance and their relationship to cognition remains unknown. We aimed to determine differences in gait and balance impairments in those with and without GBA variants (mutation carriers and E326K polymorphism) and explore direct and indirect effects of GBA status on gait, balance, and cognition. 332 participants, 43 of whom had GBA variants, were recruited. Participants completed a comprehensive, objective assessment of gait and standing balance using body-worn inertial sensors. Group differences in gait and balance between PD with and without GBA variants were assessed with linear regression, adjusting for age, gender, clinical testing site, disease duration, and apolipoprotein E (APOE) ɛ4 status. Structural equation modeling (SEM) explored direct relationships between GBA status and gait and balance and indirect relationships between GBA status and gait and balance via cognition. The GBA variant group had more impaired gait (pace and variability) and balance (sway area/jerk and sway velocity), than the non-GBA variant group. SEM demonstrated cognition as a mediator of GBA status on gait and balance. The close relationships among GBA, gait/balance, and cognition suggest potential for novel therapeutics to target the GBA pathway and/or cognition to improve mobility in PD GBA variants.

Identifiers

PMID35725575
PMCPMC9209443
OpenAlexW4283170853

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.