Evidence map›Paper›PMID 18752982›Full record

ArticleParkinsonism & related disorders2009

LRRK2 gene G2019S mutation and SNPs [haplotypes] in subtypes of Parkinson's disease.

Biswanath Patra, Azemat J Parsian, Brad A Racette, Jing Hua Zhao, Joel S Perlmutter, Abbas Parsian

Abstract read
In one paragraph

Article in Parkinsonism & related disorders, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

5 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. A Comprehensive Analysis of Population Differences inFrontiers in aging neuroscience · 2019
    Article
  3. Article
  4. Article
  5. The LRRK2 G2019S mutation as the cause of Parkinson's disease in Ashkenazi Jews.Journal of neural transmission (Vienna, Austria : 1996) · 2009
    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

6 authors at 3 institutions in 2 countries.

Biswanath PatraSimmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA.
Azemat J Parsian
Brad A Racette
Jing Hua Zhao
Joel S Perlmutter
Abbas Parsian
Washington University in St. Louis · USUniversity of Arkansas for Medical Sciences · USThe University of Texas Southwestern Medical Center · US

Funding

MECHANISMS OF DEEP BRAIN STIMULATIONR01NS041509 · NINDS · WASHINGTON UNIVERSITY · PI PERLMUTTER, JOEL SYNES · 2001 to 2015
$6.8M
VALIDATION OF NEUROIMAGING BIOMARKERS FOR NIGROSTRIATAL NEURONSR01NS058714 · NINDS · WASHINGTON UNIVERSITY · PI PERLMUTTER, JOEL SYNES · 2008 to 2016
$4.4M
CARBOXYFULLERENE TREATMENT OF MPTP-INDUCED PARKINSONISMR01NS050425 · NINDS · WASHINGTON UNIVERSITY · PI PERLMUTTER, JOEL SYNES · 2005 to 2009
$2.6M
QTL Mapping in Inbred FH Rat Strain for Alcohol IntakeR21AA014247 · NIAAA · ARKANSAS CHILDREN'S HOSPITAL RES INST · PI PARSIAN, ABBAS · 2005 to 2007
$345k
NIAAA NIH HHS R21 AA014247NINDS NIH HHS R01 NS041509NINDS NIH HHS R01 NS050425NINDS NIH HHS R01 NS058714
6 · The paper itself

Abstract

Mutation within the leucine-rich repeat kinase 2 (LRRK2) gene has been identified as a cause of autosomal dominant Parkinson's disease (PD). The purpose of this study was to determine the frequency of G2019S mutation and whether the differences in the allele and genotype distribution of six SNPs within LRRK2 gene are associated with PD in an American non-Hispanic white population. The sample included 350 sporadic PD (SPD), 225 familial PD (FPD) patients and 186 controls of the same race and ethnicity. The frequency of LRRK2 G2019S mutation in our total sample of PD (FPD and SPD) was 1.56%. The frequency of this mutation was 3.5% in the FPD and 0.3% in the SPD groups, respectively. Allele and genotype frequencies of six SNPs were compared between PD and control samples. In addition, PD groups were categorized by sporadic PD (no family history), familial PD (first degree relative with PD) and age of onset (AON, <or=50 or >or=51years). The haplotypes of the six SNPs were also constructed for association analysis. After correction for multiple comparisons, there was no association between any SNPs (allele or genotype) and PD groups. One of the haplotypes was modestly associated with the combined PD (SPD and FPD) sample. There was also no association with age at onset of PD. Our study suggests that the LRRK2 gene may be a risk factor or the cause for a very small fraction of PD in American white population.

Indexed as

Genetic Predisposition to DiseaseAgedAged, 80 and overAge of OnsetDNA Mutational AnalysisFemaleGene FrequencyGlycineHaplotypesHumansLeucine-Rich Repeat Serine-Threonine Protein Kinase-2MaleMiddle AgedParkinson DiseasePolymorphism, Single NucleotideProtein Serine-Threonine KinasesGlycineLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, humanProtein Serine-Threonine KinasesSerine

Identifiers

PMID18752982
PMCPMC2761091
OpenAlexW2084958448

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Registered trials

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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.