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LRRK2 at the interface of autophagosomes, endosomes and lysosomes

Dorien A Roosen1,2, Mark R Cookson3

  • 1Cell Biology and Gene Expression Section, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bldg. 35, 35 Convent Drive, Bethesda, MD, 20892-3707, USA.

Molecular Neurodegeneration
|December 9, 2016
PubMed

Insights

Genetic mutations in LRRK2 are a significant cause of Parkinson's disease (PD). Research suggests LRRK2 influences vesicular dynamics, offering potential therapeutic targets for PD.

Area of Science:

  • Neurogenetics
  • Cellular Biology
  • Molecular Medicine

Background:

  • Parkinson's disease (PD) genetics research has identified LRRK2 as a major contributor.
  • The precise function of LRRK2 in PD pathogenesis remains unclear.
  • Familial PD cases suggest a role for endomembrane trafficking in disease development.

Purpose of the Study:

  • To review the role of LRRK2 in Parkinson's disease.
  • To explore the connection between LRRK2, endomembrane trafficking, and vesicular dynamics.
  • To identify potential therapeutic strategies targeting LRRK2 pathways.

Main Methods:

  • Review of existing literature on LRRK2 genetics and PD.
  • Analysis of findings from LRRK2 animal models.
  • Examination of high-throughput proteomics data.

Main Results:

  • Studies strongly implicate LRRK2 in regulating vesicular dynamics.
  • Alterations in endomembrane trafficking are hypothesized to be central to PD pathobiology.
  • LRRK2's function is closely linked to cellular transport mechanisms.

Conclusions:

  • LRRK2 plays a critical role in vesicular dynamics, impacting Parkinson's disease.
  • Targeting LRRK2-associated pathways may offer therapeutic benefits for various PD forms.
  • Understanding LRRK2's function is key to developing novel PD treatments.
Keywords:
GTPasesMembrane proteinsParkinson’s diseaseProtein kinasesVesicular trafficking

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