Evidence map›Paper›PMID 21538530›Full record

ReviewMovement disorders : official journal of the Movement Disorder Society2011

Genetic LRRK2 models of Parkinson's disease: Dissecting the pathogenic pathway and exploring clinical applications.

Zhenyu Yue, M Lenard Lachenmayer

Open access · greenAbstract readReview
In one paragraph

Review in Movement disorders : official journal of the Movement Disorder Society, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Failure of Diphtheria Toxin Model to Induce Parkinson-Like Behavior in Mice.International journal of molecular sciences · 2021
    Article
  6. Article
  7. Article
  8. Parkinson's Disease-Associated LRRK2 Hyperactive Kinase Mutant Disrupts Synaptic Vesicle Trafficking in Ventral Midbrain Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. LRRK2 R1441G mice are more liable to dopamine depletion and locomotor inactivity.Annals of clinical and translational neurology · 2014
    Article
  15. Review
  16. Article
  17. Animal models of Parkinson's disease: limits and relevance to neuroprotection studies.Movement disorders : official journal of the Movement Disorder Society · 2013
    Review
  18. Article
  19. Review
  20. 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

2 authors at 1 institution in 2 countries.

Zhenyu YueDepartment of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, New York, USA. zhenyu.yue@mssm.edu
M Lenard Lachenmayer
Icahn School of Medicine at Mount Sinai · US

Funding

Using BAC-transgenic and Proteomic Approach to Study LRRK2 Biology and PathologyR01NS060809 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI YUE, ZHENYU · 2008 to 2017
$4.2M
Cellular and Molecular Basis for Initial PD Pathogenic Events in LRRK2 BAC ModelsR01NS072359 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BLITZER, ROBERT D., YUE, ZHENYU · 2011 to 2015
$1.8M
LRRK2 Proteomics: Kinase/GTPase Hypothesis and Interaction PartnersR21NS055683 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI YUE, ZHENYU · 2006 to 2007
$414k
Exploration of motor deficits and cognitive impairments in LRRK2 transgenic miceR21NS061152 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI YUE, ZHENYU, ZHOU, QIANG · 2008 to 2009
$408k
NINDS NIH HHS NS060809-01NINDS NIH HHS R01 NS060809NINDS NIH HHS R01 NS072359NINDS NIH HHS R21 NS055683NINDS NIH HHS R21 NS061152
6 · The paper itself

Abstract

Dominantly inherited mutations in leucine-rich repeat kinase 2 are the most common cause of familial Parkinson's disease. Understanding leucine-rich repeat kinase 2 biology and pathophysiology is central to the elucidation of Parkinson's disease etiology and development of disease intervention. Recently, a number of genetic mouse models of leucine-rich repeat kinase 2 have been reported utilizing different genetic approaches. Some similarities in Parkinson's disease-related pathology emerge in these genetic models despite lack of substantial neuropathology and clinical syndromes of Parkinson's disease. The systematic characterization of these models has begun to shed light on leucine-rich repeat kinase 2 biology and pathophysiology and is expected to offer the identification and validation of drug targets. In this review, we summarize the progress of genetic leucine-rich repeat kinase 2 mouse models and discuss their utility in understanding much needed knowledge regarding early-stage (presymptomatic) disease progression, identifying drug targets, and exploring the potential to aid compound screening focused on inhibitors of kinase activity of leucine-rich repeat kinase 2.

Indexed as

Parkinson Diseasealpha-SynucleinAnimalsAntiparasitic AgentsDisease Models, AnimalGene Expression RegulationHumansLeucine-Rich Repeat Serine-Threonine Protein Kinase-2MiceMice, TransgenicMutationNerve DegenerationNeurogliaProtein Serine-Threonine Kinasestau Proteinsalpha-SynucleinAntiparasitic AgentsLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, humanProtein Serine-Threonine Kinasestau Proteins

Identifiers

PMID21538530
PMCPMC3150637
OpenAlexW2159216848

What OpenQuestion holds

Textmetadata
LicenceTDM
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.