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Related Experiment Video

Updated: Jun 19, 2026

Assaying the Kinase Activity of LRRK2 in vitro

Assaying the Kinase Activity of LRRK2 in vitro

Published on: January 18, 2012

Lrrk2 interaction with alpha-synuclein in diffuse Lewy body disease.

Hong Qing¹, Yanyan Zhang, Yulin Deng

¹Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3.

Biochemical and Biophysical Research Communications

|November 3, 2009

Summary

Mutations in leucine-rich repeat kinase 2 (LRRK2) and alpha-synuclein are linked to Parkinson's disease (PD). This study found LRRK2 and alpha-synuclein interact, especially under oxidative stress, suggesting new therapeutic targets for PD.

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Last Updated: Jun 19, 2026

Assaying the Kinase Activity of LRRK2 in vitro

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Published on: January 18, 2012

Metabolic Labeling of Leucine Rich Repeat Kinases 1 and 2 with Radioactive Phosphate

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Published on: September 18, 2013

Rab10 Phosphorylation Detection by LRRK2 Activity Using SDS-PAGE with a Phosphate-binding Tag

Rab10 Phosphorylation Detection by LRRK2 Activity Using SDS-PAGE with a Phosphate-binding Tag

Published on: December 14, 2017

Area of Science:

Neuroscience
Genetics
Cell Biology

Background:

Mutations in leucine-rich repeat kinase 2 (LRRK2) are a primary genetic cause of Parkinson's disease (PD) and diffuse Lewy body disease (DLB).
Both LRRK2 and alpha-synuclein mutations are associated with autosomal dominant neurodegenerative disorders.
A gain-of-function mechanism is suggested for LRRK2 mutations in PD pathogenesis.

Purpose of the Study:

To investigate the interaction between LRRK2 and alpha-synuclein in diffuse Lewy body disease (DLB) and under oxidative stress conditions.
To explore the potential role of LRRK2-alpha-synuclein interaction in the pathogenesis of Parkinson's disease and related synucleinopathies.

Main Methods:

Co-immunoprecipitation assays using soluble brain extracts from DLB cases and controls.
Double immunostaining of postmortem DLB brain tissue to detect colocalization of LRRK2 and alpha-synuclein.
Oxidative stress induction using hydrogen peroxide (H2O2) in HEK cells co-expressing LRRK2 and alpha-synuclein, followed by co-immunoprecipitation.

Main Results:

LRRK2 and alpha-synuclein co-immunoprecipitated in all five DLB cases but not in controls.
Colocalization of LRRK2 and alpha-synuclein was observed in pathological deposits in DLB brains.
Oxidative stress in HEK cells promoted co-immunoprecipitation of LRRK2 and alpha-synuclein.

Conclusions:

The findings suggest a pathological interaction between LRRK2 and alpha-synuclein in DLB.
Oxidative stress may upregulate LRRK2 and alpha-synuclein expression, facilitating their interaction in PD and synucleinopathies.
Targeting the LRRK2-alpha-synuclein interaction could offer novel therapeutic strategies for PD and related disorders.