Jerome Mertens, PhD

Throughout my scientific career, my focus was on studying neurological disorders and brain aging by using human stem cell and reprogramming technologies, paired with cellular and molecular neuroscience. My research as a graduate student under the supervision of Oliver Brüstle at the University of Bonn in Germany provided me with a solid foundation in neurodegeneration, human pluripotent stem cell biology, and reprogramming techniques. Back then, we devised some of the earliest studies on the use of human pluripotent stem cells, both transgenic embryonic stem cells and iPSCs, to model and study AD. One of our major findings was that human stem cell-derived neurons possess a specific responsiveness towards potential drugs, and that these cells are more predictive than commonly used cancer cell. As a postdoctoral researcher at the Salk Institute under the supervision of Rusty Gage, I was fortunate to have the environment and support to strengthen my experimental skills in neuroscience, next-generation sequencing and bioinformatics analysis of big biological data sets. Combining my expertise in iPSCs biology with functional cellular neuroscience we could show how lithium affects the intrinsic hyperexcitability of Bipolar Disorder patient-derived neurons. Further, based on my long lasting interest in the study of age-related neurodegeneration, I initiated a project that showed that direct conversion of fibroblasts in induced neurons (iNs) preserves signatures of cellular aging, while iPSC reprogramming erases them. Follow-up work on iNs from my new lab in Innsbruck in collaboration with the Gage lab, as well as from several other labs around the globe has now further extended our knowledge and revealed how the nuclear pore, mitochondria, protein homeostasis, and epigenetic aging signatures are reflected in iNs, together rendering the iN system as a unique, patient-specific, and ‘age-equivalent’ neuronal model for human diseases. My overall research goal is to harness my expertise in cell biology, neuroscience, and systems biology to fully exploit the iN system to unravel the molecular key players that define progressive human cellular age and set the stage for age-related neurodegenerative diseases. My work aims to contribute to finding new personalized diagnostics and treatments that may target pathogenic mechanisms of age-related neurodegenerative disease, specifically sporadic AD.