Laurie H. Sanders

This study identifies Rab12 as a negative regulator of mitophagy and mitochondrial homeostasis, showing its loss increases mitochondrial clearance and sensitivity to stress.

This study shows that the LRRK2 G2019S mutation causes oxidative nuclear DNA damage and PARP1 hyperactivation, leading to cellular vulnerability in Parkinson's disease.

This study shows that LRRK2-mediated phosphorylation of Rab12 accumulates in lysosomal-like structures in tauopathies and synucleinopathies, linking LRRK2 kinase activity to endolysosomal dysfunction.

The paper measures LRRK2 kinase activity via pT73-Rab10 in serum, linking it to inflammation and Parkinson's disease severity.

The paper tests a G2019S selective LRRK2 inhibitor, EB-42168, showing it reduces mtDNA damage in G2019S models and patient cells better than a non-selective inhibitor.

This study uses CRISPRi to downregulate alpha-synuclein in a Parkinson's disease patient-derived model, reducing oxidative stress and mtDNA damage.

The paper identifies mtDNA damage as a blood-based biomarker for Parkinson's disease, showing increased levels in early-stage patients and mutation carriers, suggesting its potential for patient stratification in clinical trials.