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Parkinson's disease and immune system: is the culprit LRRKing in the periphery?

Elisa Greggio1, Laura Civiero, Marco Bisaglia

  • 1Department of Biology, University of Padova, Via Ugo Bassi 58/B, Padova, 35121, Italy. elisa.greggio@unipd.it

Journal of Neuroinflammation
|May 19, 2012
PubMed

Insights

Leucine-rich repeat kinase 2 (LRRK2) impacts immune responses and is linked to Parkinson's disease. LRRK2 mutations may cause peripheral inflammation that affects the central nervous system.

Area of Science:

  • Biochemistry
  • Immunology
  • Neuroscience

Background:

  • Leucine-rich repeat kinase 2 (LRRK2) is a kinase/GTPase implicated in Parkinson's disease, Crohn's disease, and leprosy.
  • LRRK2's role in inflammation is suggested by its expression in immune cells and regulation of immune factors.

Purpose of the Study:

  • To review recent findings on LRRK2's role in inflammatory responses.
  • To propose a model for how LRRK2 mutations contribute to Parkinson's disease pathogenesis via peripheral inflammation.

Main Methods:

  • Literature review of LRRK2 function and disease associations.
  • Analysis of LRRK2's interaction with immune pathways and its regulation by inflammatory signals.

Main Results:

  • LRRK2 is highly expressed in immune cells and upregulated by interferon-gamma.
  • LRRK2 negatively regulates the immune transcription factor NFAT1.
  • Evidence suggests LRRK2 influences peripheral inflammatory processes.

Conclusions:

  • LRRK2 plays a significant role in the immune response.
  • Parkinson's disease-associated LRRK2 mutations may initiate pathology in the periphery.
  • Peripheral inflammation driven by LRRK2 mutations could impact the central nervous system via the blood-brain barrier.

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