Dr. Ferguson earned BSc (Biochemistry-Nutrition) and MSc (Physiology) degrees from the University of Ottawa followed by a PhD in Neuroscience from Vanderbilt University in 2004. From 2004-2010, he was a postdoctoral fellow with Pietro De Camilli in the Department of Cell Biology at Yale. As a postdoctoral fellow, he studied the membrane trafficking mechanisms that allow neurons to make and recycle the synaptic vesicles which are used for the storage and release of neurotransmitters that support communication between neurons. Although centered on the topic of neuronal cell biology, this research resulted in many additional collaborative studies that focused on how similar membrane trafficking mechanisms are adapted to the needs of other cell types. In 2010, Dr. Ferguson was recruited into a faculty position in the Department of Cell Biology at Yale where he currently holds the rank of Associate Professor (tenured). The long-term goal of research in the Ferguson lab is to understand the cell biological mechanisms that allow neurons to meet the challenges imposed by their extreme size, polarity, longevity and specialized membrane trafficking demands related to synaptic transmission. Given the major role played by lysosomes in supporting neuronal health through the clearance of misfolded proteins and damaged organelles, the lab has focused significant efforts to understand how the status of lysosomes is sensed and how cells respond to ensure that lysosome function meets ongoing changes in cellular demand. The ability of lysosomes to degrade misfolded proteins and damaged organelles is of critical importance for neuronal survival as defects in such processes contribute to the development of multiple neurodegenerative diseases. Ongoing neurodegenerative disease projects in the lab address the role of lysosomes in Alzheimer’s disease, amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and Parkinson’s disease. More recently, the identification of human mutations in the MAPK8IP3, a gene studied by the Ferguson lab in the context of axonal transport of lysosomes within neurons, was identified as the cause of a human neurodevelopmental disorder. To address this problem, Dr. Ferguson and his team are working with The Wolverine Foundation to advance research and discover novel therapeutic approaches to treat the neuro-developmental disease caused by genetic variations in the gene MAPK8IP3. In particular, the Ferguson Lab uses human neurons derived from induced pluripotent stem cells (iPSCs) as a platform for the identification of candidate therapeutic strategies to treat disabilities arising from MAPK8IP3 deficiency.