Evidence map›Paper›PMID 23938341›Full record

ReviewJournal of Parkinson's disease2013

LRRK2: cause, risk, and mechanism.

Coro Paisán-Ruiz, Patrick A Lewis, Andrew B Singleton

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of Parkinson's disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
4.5field-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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 154 citations in OpenAlex.

  1. A systematic review of molecular approaches that link mitochondrial dysfunction and neuroinflammation in Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Exploring LRRK2-dependent Mechanisms in Parkinson's Disease Therapy.CNS & neurological disorders drug targets · 2025
    Review
  11. Article
  12. Leucine-rich repeat kinase 2 limits dopamine D1 receptor signaling in striatum and biases against heavy persistent alcohol drinking.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

25 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 2 countries.

Coro Paisán-RuizDepartment of Neurology, Psychiatry, and Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, NY, USA.
Patrick A Lewis
Andrew B Singleton
Allen Institute for Brain Science · USNational Institute on Aging · USQueen Mary University of London · GB

Funding

Assessment of Candidate Loci in Neurological diseasesZIAAG000957 · NIA · NATIONAL INSTITUTE ON AGING · PI SINGLETON, ANDREW · 2009 to 2024
$12.2M
Genome wide SNP analysis in Parkinson's diseaseZ01AG000949 · NIA · NATIONAL INSTITUTE ON AGING · PI SINGLETON, ANDREW B · 2006 to 2008
$2.6M
Elucidating and understanding the genetic basis of movement disordersR01NS079388 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI PAISAN-RUIZ, CORO · 2013 to 2017
$1.9M
Whole Genome Screen in families with Parkinson's diseaseZ01AG000958 · NIA · NATIONAL INSTITUTE ON AGING · PI SINGLETON, ANDREW B · 2003 to 2008
$1.4M
Intramural NIH HHS Z01 AG000949Intramural NIH HHS Z01 AG000958Medical Research CouncilNIA NIH HHS ZO1 AG000949-07NIA NIH HHS ZO1 AG000958-10NINDS NIH HHS R01 NS079388NINDS NIH HHS R01NS079388Wellcome TrustWellcome Trust WT089698
6 · The paper itself

Abstract

In 2004 it was first shown that mutations in LRRK2 can cause Parkinson's disease. This initial discovery was quickly followed by the observation that a single particular mutation is a relatively common cause of Parkinson's disease across varied populations. Further genetic investigation has revealed a variety of genetic ties to Parkinson's disease across this gene. These include common alleles with quite broad effects on risk, likely through both alterations at the protein sequence level, and in the context of expression. A great deal of functional characterization of LRRK2 and disease-causing mutations in this protein has occurred over the last 9 years, and considerable progress has been made. Particular attention has been paid to the kinase activity of LRRK2 as a therapeutic target, and while it is no means certain that this is viable target it is likely that this hypothesis will be tested in clinical trials sooner rather than later. We believe that the future goals for LRRK2 research are, while challenging, relatively clear and that the next 10 years of research promises to be perhaps more exciting than the last.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseaseHumansLeucine-Rich Repeat Serine-Threonine Protein Kinase-2MutationParkinson DiseaseProtein Serine-Threonine KinasesLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, humanProtein Serine-Threonine Kinases

Identifiers

PMID23938341
PMCPMC3952583
OpenAlexW1611134798

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.