Dr. LaVoie has been an Associate Professor of Neurology at Brigham and Women’s Hospital and Harvard Medical School since 2012. He has been actively investigating the causes of age-related neurodegenerative disease since he was an undergraduate at Rutgers College. His interest in these devastating disorders took him to the University of Pittsburgh for graduate training, where he had the opportunity to work not only with world-class scientists, but also with patients and patient-advocates towards passage of the Morris K. Udall act into law in 1997, the first federal legislation to earmark special funding for research in Parkinson’s disease. He continued to expand his training during a postdoctoral fellowship in Alzheimer’s disease at the Brigham, where he made seminal contributions to our understanding of presenilin, the protein responsible for the production of amyloid beta peptide. In his independent lab, he expanded his efforts to focus on uncovering the primary triggers of neurodegeneration in Parkinson’s disease. Dr. LaVoie continues to support the Parkinson’s community both nationally and internationally through service on the Scientific Advisory Board of the Parkinson Foundation, the National Scientific Advisory Council of the American Federation for Aging Research, and support of the Michael J. Fox Foundation and the Parkinson’s Society UK. He has received numerous awards for his contributions to neurodegenerative disease research including being named a World Parkinson’s Junior Scholar in 2006, receiving the Roberto Cornelli award in 2007, and several other honors. He currently serves on the Editorial Board of The Journal of Parkinson’s Disease and is Editor-in-Chief of Brain Research, a journal serving the neuroscience community for over 50 years.
Dr. LaVoie is particularly dedicated to understanding the earliest molecular events that initiate Parkinson’s disease (PD). To gain a better understanding of this complex neurodegenerative disorder, the LaVoie lab take cues from inherited forms of PD, where they study discrete genetic mutations that cause disease. For example, mutations within the large kinase LRRK2 are the most common genetic cause of PD. Having already made important discoveries on the function of LRRK2, Dr. LaVoie has teamed up with leading neuro-immunologists and pathologists to understand how these mutations influence the human nervous system. As LRRK2 is a primary pharmacologic target for disease-modification in PD, the lab is also keenly interested in the effects of small molecule inhibitors of LRRK2, and their potential utility beyond LRRK2 carriers. The LaVoie lab has also made numerous contributions to our understanding of how mutations in a protein named ‘parkin’ disturb mitochondrial function and promote neuronal cell death. A new line of promising research has begun to study critical overlaps between inherited mitochondrial disorders and PD, to identify the links between mitochondrial dysfunction and PD-like pathology. With this balanced approach of studying both inherited and sporadic forms of PD, the LaVoie lab hopes to identify the factors that initiate neuronal dysfunction and cell loss in PD for the targeted development of disease-modifying and preventative therapeutics. Along with his primary role as lab director, Dr. LaVoie is also a committed medical educator. He has been invited to teach at Simmons College, Brandeis University, Harvard College, and served as the Co-Director for the preclinical curriculum in Neurology and Neuroanatomy for Harvard Medical School from 2012-2016.