Evidence map›Paper›PMID 27402877›Full record

ArticleHuman molecular genetics2016

Identification of genetic modifiers of age-at-onset for familial Parkinson's disease.

Erin M Hill-Burns, Owen A Ross, William T Wissemann, Alexandra I Soto-Ortolaza, Sepideh Zareparsi, Joanna Siuda, Timothy Lynch, Zbigniew K Wszolek, Peter A Silburn, George D Mellick and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

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  12. Molecules and cells · 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

16 authors at 12 institutions in 4 countries.

Erin M Hill-BurnsDepartment of Neurology, University of Alabama at Birmingham, AL, USA.
Owen A RossDepartment of Neuroscience, Mayo Clinic Jacksonville, FL, USA.
William T WissemannDepartment of Neurology, University of Alabama at Birmingham, AL, USA.
Alexandra I Soto-OrtolazaDepartment of Neuroscience, Mayo Clinic Jacksonville, FL, USA.
Sepideh ZareparsiDepartment of Molecular and Medical Genetics, Oregon Health & Sciences University, Portland, OR, USA.
Joanna SiudaDepartment of Neurology, Medical University of Silesia, Katowice, Poland.
Timothy LynchDublin Neurological Institute at the Mater Misericordiae University Hospital, Conway Institute of Biomolecular & Biomedical Research, University College Dublin, Ireland.
Zbigniew K WszolekDepartment of Neurology, Mayo Clinic Jacksonville, FL, USA.
Peter A SilburnEskitis Institute for Drug Discovery, Griffith University, Queensland, Australia.
George D MellickEskitis Institute for Drug Discovery, Griffith University, Queensland, Australia.
Beate RitzDepartment of Epidemiology, Fielding School of Public Health and Neurology, Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Clemens R ScherzerThe Neurogenomics Laboratory, Harvard Medical School and Brigham & Women's Hospital, Cambridge, MA, USA.
Cyrus P ZabetianVA Puget Sound Health Care System and Department of Neurology, University of Washington, Seattle, WA, USA.
Stewart A FactorDepartment of Neurology, Emory University School of Medicine, Atlanta, GA, USA.
Patrick J BrehenyDepartment of Biostatistics, University of Iowa, Iowa City, IA, USA.
Haydeh PayamiDepartment of Neurology, University of Alabama at Birmingham, AL, USA haydehpayami@uabmc.edu.
Griffith University · AUMayo Clinic in Florida · USUniversity of Alabama at Birmingham · USBrigham and Women's Hospital · USEmory University · USHudsonAlpha Institute for Biotechnology · USMedical University of Silesia · PLOregon Health & Science University · USUniversity College Dublin · IEUniversity of Iowa · USVA Puget Sound Health Care System · USWinnMed · US

Funding

THE ROLE OF ADVANCED CAA IN ALZHEIMER'S DEMENTIAP50AG005134 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 1985 to 2018
$42.1M
Outreach, Recruitment and Education CoreP30AG008017 · NIA · OREGON HEALTH & SCIENCE UNIVERSITY · PI BOISE, LINDA · 1990 to 2019
$27.7M
Neuropathology CoreP50NS072187 · NINDS · MAYO CLINIC JACKSONVILLE · PI DICKSON, DENNIS WILLIAM · 2010 to 2017
$8.7M
Center for Gene-Environment Studies in Parkinson DiseaseU54ES012078 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHESSELET, MARIE-FRANCOISE S · 2002 to 2006
$7.1M
PARKINSON'S DISEASES SUSCEPTIBILITY GENES AND PESTICIDESR01ES010544 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI RITZ, BEATE R. · 2000 to 2015
$5.7M
GENETIC ANALYSIS OF ONSET AGE OF PARKINSONS DISEASER01NS036960 · NINDS · WADSWORTH CENTER · PI PAYAMI, HAYDEH · 1998 to 2012
$3.9M
Biomarkers for early intervention in Parkinson diseaseU01NS082157 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI SCHERZER, CLEMENS R · 2012 to 2016
$2.5M
Understanding the role of MAPT in Parkinsonian disordersR01NS078086 · NINDS · MAYO CLINIC JACKSONVILLE · PI ROSS, OWEN A · 2012 to 2016
$1.7M
Genetic Risk Factors for Parkinson's DiseaseI01BX000531 · VA · VA PUGET SOUND HEALTHCARE SYSTEM · PI ZABETIAN, CYRUS P · 2009 to 2013
–
BLRD VA I01 BX000531NHGRI NIH HHS HHSN268200782096CNIA NIH HHS P30 AG008017NIA NIH HHS P50 AG005134NIEHS NIH HHS R01 ES010544NIEHS NIH HHS U54 ES012078NINDS NIH HHS P50 NS072187NINDS NIH HHS R01 NS036960NINDS NIH HHS R01 NS078086NINDS NIH HHS U01 NS082157
6 · The paper itself

Abstract

Parkinson's disease (PD) is the most common cause of neurodegenerative movement disorder and the second most common cause of dementia. Genes are thought to have a stronger effect on age-at-onset of PD than on risk, yet there has been a phenomenal success in identifying risk loci but not age-at-onset modifiers. We conducted a genome-wide study for age-at-onset. We analysed familial and non-familial PD separately, per prior evidence for strong genetic effect on age-at-onset in familial PD. GWAS was conducted in 431 unrelated PD individuals with at least one affected relative (familial PD) and 1544 non-familial PD from the NeuroGenetics Research Consortium (NGRC); an additional 737 familial PD and 2363 non-familial PD were used for replication. In familial PD, two signals were detected and replicated robustly: one mapped to LHFPL2 on 5q14.1 (P

Indexed as

AgedAged, 80 and overAge of OnsetFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMaleMembrane ProteinsMiddle AgedParkinson DiseasePolymorphism, Single NucleotideProteinsTropomyosinLHFPL2 protein, humanMembrane ProteinsProteinsTPM1 protein, humanTropomyosin

Identifiers

PMID27402877
PMCPMC5216611
OpenAlexW2460686087

What OpenQuestion holds

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LicenceCC BY-NC
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.