Evidence map›Paper›PMID 33423828›Full record

ArticleNeurobiology of aging2021

Assessment of LIN28A variants in Parkinson's disease in large European cohorts.

Monica Diez-Fairen, Mary B Makarious, Sara Bandres-Ciga, Cornelis Blauwendraat, International Parkinson's Disease Genomics Consortium (IPDGC)

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

Article in Neurobiology of aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 31% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
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

5 authors at 3 institutions in 2 countries.

Monica Diez-FairenDepartment of Neurology, Fundació Docència i Recerca MútuaTerrassa and Movement Disorders Unit, University Hospital MútuaTerrassa, Terrassa, Barcelona, Spain.
Mary B MakariousMolecular Genetics Section, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA.
Sara Bandres-CigaMolecular Genetics Section, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA.
Cornelis BlauwendraatMolecular Genetics Section, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA. Electronic address: cornelis.blauwendraat@nih.gov.
International Parkinson's Disease Genomics Consortium (IPDGC)
National Institutes of Health · USNational Institute on Aging · USUniversity Hospital Mútua de Terrassa · ES

Funding

Genetic characterization of atypical parkinsonismZIANS003154 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI SCHOLZ, SONJA · 2016 to 2025
$15.4M
Genome wide SNP analysis in Parkinson's diseaseZ01AG000949 · NIA · NATIONAL INSTITUTE ON AGING · PI SINGLETON, ANDREW B · 2006 to 2008
$2.6M
Prospective studies on Parkinson's diseaseZ01ES101986 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI CHEN, HONGLEI · 2006 to 2008
$1.2M
Intramural NIH HHS Z01 AG000949Intramural NIH HHS Z01 ES101986Intramural NIH HHS Z99 AG999999Intramural NIH HHS ZIA NS003154
6 · The paper itself

Abstract

Parkinson's disease (PD) is a complex neurodegenerative disease with a strong genetic component. To date, several genes have been associated with monogenic forms of the disease, but these only explain a small fraction of the observed familial aggregation in PD. Recently, a heterozygous loss-of-function variant in LIN28A was associated with PD pathogenesis in the Asian population. Here, we comprehensively investigate the role of LIN28A variants in PD patients of European ancestry and assess susceptibility using individual-level genotyping data from 14,671 PD cases and 17,667 controls, as well as whole-genome sequencing data from 1647 patients with PD and 1050 controls. In addition, we further assess the summary statistics from the most recent genome-wide association studies meta-analyses to date for PD risk and age at onset. After evaluating these data, we did not find evidence to support a role for LIN28A as a major causal gene for PD. However, additional large-scale familial and case-control studies in non-European ancestry populations are necessary to further evaluate the role of LIN28A in PD etiology.

Indexed as

Genome-Wide Association StudyNegative ResultsAgedAge of OnsetCohort StudiesDatabases, GeneticData Interpretation, StatisticalGenetic Predisposition to DiseaseHumansLoss of Function MutationMaleMeta-Analysis as TopicMiddle AgedParkinson DiseaseRisk FactorsRNA-Binding ProteinsLin28A protein, humanRNA-Binding ProteinsLIN28ALoss of functionParkinson's diseaseRisk factor

Identifiers

PMID33423828
PMCPMC7920911
OpenAlexW3113344914

What OpenQuestion holds

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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.