Evidence map›Paper›PMID 22361010›Full record

ReviewBMC medicine2012

Is inhibition of kinase activity the only therapeutic strategy for LRRK2-associated Parkinson's disease?

Iakov N Rudenko, Ruth Chia, Mark R Cookson

Abstract readReview
In one paragraph

Review in BMC medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
–field-weighted citation impact
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

36 citing papers in PubMed.

  1. Review
  2. Article
  3. LRRK2 and Proteostasis in Parkinson's Disease.International journal of molecular sciences · 2022
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Allosteric inhibition of LRRK2, where are we now.Biochemical Society transactions · 2020
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Roco Proteins and the Parkinson's Disease-Associated LRRK2.International journal of molecular sciences · 2018
    Review
  15. Review
  16. LRRK2 promotes the activation of NLRC4 inflammasome duringThe Journal of experimental medicine · 2017
    Article
  17. Article
  18. Review
  19. Review
  20. 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

3 authors.

Iakov N RudenkoCell Biology and Gene Expression Section, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, 35 Convent Drive, Room 1A-116, Bethesda, MD 20892-3707, USA.
Ruth Chia
Mark R Cookson

Funding

GTPase function of Leucine rich repeat kinase 2ZIAAG000937 · NIA · NATIONAL INSTITUTE ON AGING · PI COOKSON, MARK · 2010 to 2025
$9.2M
Intramural NIH HHS
6 · The paper itself

Abstract

Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are a common cause of familial Parkinson's disease (PD). Variation around the LRRK2 locus also contributes to the risk of sporadic PD. The LRRK2 protein contains a central catalytic region, and pathogenic mutations cluster in the Ras of complex protein C terminus of Ras of complex protein (mutations N1437H, R1441G/C and Y1699C) and kinase (G2019S and I2020T) domains. Much attention has been focused on the kinase domain, because kinase-dead versions of mutant LRRK2 are less toxic than kinase-active versions of the same proteins. Furthermore, kinase inhibitors may be able to mimic this effect in mouse models, although the currently tested inhibitors are not completely specific. In this review, we discuss the recent progress in the development of specific LRRK2 kinase inhibitors. We also discuss non-kinase-based therapeutic strategies for LRRK2-associated PD as it is possible that different approaches may be needed for different mutations.

Indexed as

AnimalsClinical Trials as TopicHumansMutationParkinson DiseaseProtein Kinase InhibitorsProtein Serine-Threonine KinasesTranslational Research, BiomedicalProtein Kinase InhibitorsProtein Serine-Threonine Kinases

Identifiers

PMID22361010
PMCPMC3308210

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.