Dr. Hilal A. Lashuel received his B.Sc. degree in chemistry from Brooklyn College-City University of New York in 1994 and completed his doctoral studies at Texas A&M University and the Scripps Research Institute in 2000. After obtaining his doctoral degree, he joined the Picower Institute for Medical Research in Long Island New York as a research. In 2001, he moved to Harvard Medical School and the Brigham and Women's Hospital as a research fellow in the Center for Neurologic Diseases and was later promoted to an instructor in neurology at Harvard Medical School. In 2005 Dr. Lashuel moved Switzerland to join the Brain Mind Institute at the Swiss Federal Institute of Technology Lausanne (École polytechnique fédérale de Lausanne, EPFL) as a tenure-track assistant professor in neurosciences. Currently, Dr. Lashuel is an associate professor of life sciences and the director of the laboratory of molecular and chemical biology of neurodegeneration. (http://lashuel-lab.epfl.ch/).
In addition to his appointment at the EPFL, Dr. Lashuel was a visiting Associate Professor at the Department of Neurology and Neurological Sciences at Stanford University (2012-2013) and served as the Executive Director of Qatar Biomedical Research Institute (QBRI) and a Professor at Hamad Bin Khalifa University from March 2014 – March 2016. He is also the chief scientific officer of ND BioSciences SA, a biotechnology company that he founded with the mission of developing and providing innovative technologies, solutions, tools, assays, and services to accelerate the development of early diagnostics and therapies for neurodegenerative diseases.
Several neurodegenerative diseases, including Alzheimer’s, Parkinson’s and Huntington’s disease, are characterized by the presence of misfolded and aggregated proteins in pathological inclusions or deposits in the brain regions affected by the disease. Despite more than 100 years since the identification of many of these pathological hallmarks, their mechanism of formation and their role of in the pathogenesis of these diseases remain poorly understood. This knowledge gap has significant implications for the development of 1) animal models that recapitulate the pathological and clinical features of the human disease; 2) imaging agents and biomarkers for early diagnosis and monitoring disease progression; and 3) diseases modifying strategies. Using Parkinson’s disease (PD) as an example, I will present our work aimed at addressing this knowledge gap and paving the way for developing effective diagnostic and therapeutic strategies for PD and other neurodegenerative diseases. More specifically, I will present how advances in protein chemical synthesis pioneered by our group have transformed our understanding of the role of post-translational modifications in the pathogenesis of Parkinson’s and Alzheimer’s disease. The second part of my lecture will focus on recent advances made by our group towards developing neuronal models that allow for the first reconstructing the different processes associated with the aggregation, fibrillization and the formation pathological inclusions similar to those observed in the brains of patients affected by PD. The results from these studies have provided novel insight into the mechanisms by which protein aggregation and pathology formation contribute to neuronal loss in neurodegenerative diseases. I will finish by highlighting how we are extending these approaches to reverse engineering pathology in Alzheimer’s disease and Huntington’s disease and discuss the implication of our findings for the development of effective diagnostic and disease modifying strategies for the treatment of Parkinson’s disease and other neurodegenerative disease.