During recent years, I have studied the role of lipid metabolic organelles in the model system Drosophila melanogaster. My focus is on the impact of cell organelles on the maintenance of the brain via their role in lipid metabolism and sterol trafficking, namely peroxisomes, mitochondria and lysosomes, using a combination of genetic and biochemical techniques with imaging and lipidomics approaches.
Both lysosomes and peroxisomes can be dysfunctional as a consequence of genetic defects, resulting in the development of human inherited diseases with childhood lethality. Studying these diseases, and their model system equivalents, has been contributing to our understanding of the complex roles both organelles fulfill. Furthermore, they recently emerged as important players in other diseases with much greater impact on the socio-economic burden for society. For example, both organelles play important roles in the etiology and progression of neurodegenerative diseases, like Alzheimer’s disease, and both impact the quality of mitochondria, which are in the focus of attention in the context of many neurodegenerative disorders, most prominently among them Parkinson’s disease and Alzheimer’s disease.
My current research focuses on how defective sterol trafficking contributes to neurodegeneration in Drosophila melanogaster models for lysosomal storage diseases and Alzheimer’s disease, and how mitochondrial dynamics-dependent metabolic alterations affect brain maintenance.
Unbalanced lipolysis resulting in lipotoxicity provokes mitochondrial damage in peroxisome-deficient Pex19 mutants
Dietary rescue of lipotoxicity-induced mitochondrial damage in Peroxin19 mutants
Characterization of Drosophila Saposin-related mutants as a model for lysosomal sphingolipid storage diseases