Research in our laboratory concentrates on the molecular mechanisms of neurodegeneration, with a special emphasis on the role of inflammation in Parkinson's disease. Neuroinflammatory genes have been associated with several neurodegenerative diseases, including Parkinson's disease. Our aim is to understand, at the molecular level, how disease-associated genetic variants affect immune cell metabolism, and how immune responses within or outside the brain contribute to neurodegeneration.

Another line of research concentrates on the role of GBA1 mutations in Parkinson's disease. GBA1 mutations represent the most common risk factor for Parkinson’s disease identified to date. Ongoing research in our laboratory focuses on the mechanistic pathways involved in GBA1-linked neurodegeneration, with a particular interest in mitochondrial function and autophagy. In parallel, the laboratory is exploring novel strategies to increase glucocerebrosidase activity.

We do that by combining patient neurons derived from induced pluripotent stem cells (iPSCs) and CRISPR-Cas9 genome editing techniques.