Matthew Farrer, PhD

Dr. Matt Farrer, is critically acclaimed for his work in the genetics and neuroscience of Parkinson’s disease. His inspiration to apply genetic analysis to complex neurologic disorders came from early work as a care assistant of patients and families with neurologic and psychiatric disorders. Dr. Farrer earned first degree in Biochemistry with a Doctoral degree in Molecular and Statistical Genetics from St. Mary’s Hospital Medical School, UK. He completed a Fellowship in Medical Genetics at the Kennedy-Galton Centre, UK, and in Neurogenetics at Mayo Clinic. Dr. Farrer became an Assistant Professor of Molecular Neuroscience in 2000, where he opened his first laboratory to predict and prevent Parkinson’s disease. Dr. Farrer became a tenured Professor in 2006, a Mayo Consultant and subsequently a Distinguished Mayo Investigator. In 2010, Dr. Farrer was awarded a Canada Excellence Research Chair to build the Centre for Applied Neurogenetics and Neuroscience at the University of British Columbia, Vancouver, Canada. He came a Professor of Medical Genetics. The Province of British Columbia subsequently awarded him the Don Rix Chair in Precision Medicine and his team had many notable accomplishments, including several new genes and mouse models for Parkinson’s disease. The team also implemented high-throughput sequencing in pediatric seizure disorders and neonatology in clinical service. The former was funded through the Medical Services Plan of British Columbia, and was a first for Canada.

Dr. Matt Farrer currently has appointments and affiliations in the UF College of Medicine’s Neurology Department, and the Evelyn F. and William L. McKnight Brain Institute. He is also an Adjunct Professor of the University of Saskatchewan.

My long term career objective has been to provide molecular targets, develop tools and characterize models to encourage greater pharmaceutical investment in disease-modifying therapeutics aimed at neuroprotection (‘precision medicine’). My efforts have largely been in Parkinson’s disease, to help predict and prevent this disease. My team has used linkage and comparative high-throughput sequencing in families and populations to identify many genetic contributions including the discovery of pathogenic variability in Leucine-Rich Repeat Kinase 2, Dynactin, Vacuolar Protein Sorting 35, Receptor-Mediated Endocytosis 8, Heat-Shock Protein 40 and most recently, the GTPase RAB32. Through these discoveries I appreciate the evolution of many mutations in Parkinson’s disease has been driven to deliberately attenuate the biology of lysosome-related organelles. In peripheral immune cells, such deficits in this rather specialized form of autophagy, have enabled human survival, but its vestigial role in microglia and dopamine neurons, with age, is less clear. My team also discovered alpha-synuclein gene dosage as the cause of Lewy body parkinsonism-dementia, and thus we also I maintain a keen interest in related alpha-synucleinopathies, including multiple system atrophy. We design and characterizing related cre-loxP models of mutant gene dysfunction and investigate their brain slice biochemistry and physiology, often with a focus on the dopaminergic system. We are not wedded to one technique but to a philosophy that to effectively intervene in a disease, to halt its progression and in effect provide a cure, you have to understand its molecular neuroscience and that remains a primary objective.