npj Parkinson s DiseaseNeurosciencePeer-reviewed journal article
G2019S selective LRRK2 kinase inhibitor abrogates mitochondrial DNA damage
Nicholas PenaiD, Tara Richbourg, Claudia P. González-HuntiD, Rui QiiD, Paul B. WreniD, Carrolee Barlow, Natalie F. Shanks, Holly J. CarlisleiD, Laurie H. SandersiD
Abstract
Pathogenic mutations in LRRK2 cause Parkinsons disease (PD). The G2019S variant is the most common, which results in abnormally high kinase activity. Compounds that target LRRK2 kinase activity are currently being developed and tested in clinical trials. We recently found that G2019S LRRK2 causes mitochondrial DNA (mtDNA) damage and treatment with multiple classes of LRRK2 kinase inhibitors at concentrations associated with dephosphorylation of LRRK2 reversed mtDNA damage to healthy control levels. Because maintaining the normal function of LRRK2 in heterozygous G2019S LRRK2 carriers while specifically targeting the G2019S LRRK2 activity could have an advantageous safety profile, we explored the efficacy of a G2019S mutant selective LRRK2 inhibitor to reverse mtDNA damage in G2019S LRRK2 models and patient cells relative to non-selective LRRK2 inhibitors. Potency of LRRK2 kinase inhibition by EB-42168, a G2019S mutant LRRK2 kinase inhibitor, and MLi-2, a nonselective inhibitor, was determined by measuring phosphorylation of LRRK2 at Ser935 and/or Ser1292 using quantitative western immunoblot analysis. The Mito DNADX assay, a novel system that allows for the accurate real-time quantification of mtDNA damage in a 96-well platform, was performed in parallel. We confirmed that EB-42168 selectively inhibits LRRK2 phosphorylation on G2019S LRRK2 relative to wild-type LRRK2. On the other hand, MLi-2 was equipotent for wild-type and G2019S LRRK2. Acute treatment with EB-42168 inhibited LRRK2 phosphorylation and also restored mtDNA damage to healthy control levels. Precision medicine is a common approach in modern day cancer research that is not yet routinely applied to neurodegenerative diseases. Abrogation of mtDNA damage with mutant selective tool inhibitor EB-42168 demonstrates the promise of a precision medicine approach for LRRK2 G2019S PD. Levels of mtDNA damage may serve as a potential pharmacodynamic biomarker of altered kinase activity that could be useful for small molecule development and clinical trials.
- Citations
- 33
- FWCI
- 8.03
- Field percentile
- top 2%
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- Dopaminergic Neurodegeneration Induced by Parkinson's Disease-Linked G2019S LRRK2 is Dependent on Kinase and GTPase Activity
An Phu Tran Nguyen, Elpida Tsika, … Darren J. Moore·Proceedings of the National Academy of SciencesPeer-reviewed·Jul 6, 2020
- Pharmacological rescue of impaired mitophagy in Parkinson's disease-related LRRK2 G2019S knock-in mice
F. Singh, A. R. Prescott, … I. Ganley·bioRxiv·Dec 7, 2020
- LRRK2 kinase inhibition reverses G2019S mutation-dependent effects on tau pathology spread
Noah Lubben, Julia K. Brynildsen, … Michael X. Henderson·Translational NeurodegenerationPeer-reviewed·Mar 4, 2024
- Parkinson's disease linked LRRK2 G2019S drives oxidative nuclear DNA damage and PARP1 hyperactive signaling
Jennifer Liu, Claudia P. González-Hunt, … Laurie H. Sanders·bioRxiv·Mar 1, 2026
- Parkinson's disease-associated LRRK2 risk variant, G2385R, enhances Rab substrate phosphorylation and impairs neuronal integrity
An Phu Tran Nguyen, Roger Moser, … Darren J. Moore·Human Molecular GeneticsPeer-reviewed·Jan 1, 2026
- Neurodegeneration caused by LRRK2-G2019S requires Rab10 in select dopaminergic neurons
Stavroula Petridi, C. Adam Middleton, … Christopher J. H. Elliott·bioRxiv·Mar 22, 2019