Dr. Wellington obtained her PhD at the University of British Columbia and performed postdoctoral fellowships at Harvard Medical School, the University of Calgary, and the University of British Columbia. She joined the Department of Pathology and Laboratory Medicine at the University of British Columbia in 2000 and was promoted to Professor in 2011. Dr. Wellington’s research program encompasses the genetic and environmental risk factors that affect dementia, including apolipoprotein E metabolism, history of traumatic brain injury (TBI), and cerebrovascular dysfunction. Her current research projects include drug discovery efforts to increase apolipoprotein function in the brain for application to both Alzheimer’s Disease and TBI, understanding the relationships between TBI and dementia, and innovative tissue engineering approaches to investigate cerebrovascular function in health and disease. Dr. Wellington’s niche expertise affords her a truly unique perspective. She is a highly sought-after speaker who has given well over 100 presentations in the last five years to both scientific and lay audiences and an active member of a wide range of multidisciplinary teams, committees, and grant review panels. She has served on the Editorial Board for the Journal of Lipid Research, and has demonstrated strong leadership in heading a team from the Canadian Consortium on Neurodegeneration of Aging. Dr. Wellington has published 95 peer-reviewed articles and 24 invited reviews. Her work has been cited over 6,000 times, as reflected by her h-factor of 43 (SCOPUS). In addition to her impressive body of research, Dr. Wellington is an enthusiastic mentor, and is actively engaged in service to the UBC community. She has supervised 38 research trainees, and founded a UBC Collaborative Grant Workshop Program that provides post-doctoral fellows with advanced skills in grant writing and reviewing.

Since joining UBC in 2000, my career has been focused on Alzheimer’s Disease (AD), which is the most common form of dementia in the elderly and defined by the presence of amyloid plaques and neurofibrillary tangles in the diseased brain. ApoE is the major apolipoprotein expressed in the brain and the best-established genetic risk factor for late onset AD. Using genetic and pharmacological approaches, we have shown that the amount of fats carried on apoE regulates the removal of Abeta peptides, which are neurotoxic species that accumulate as amyloid in the AD brain. This initial work has now grown to include several integrated research programs in my laboratory, all of which converge on understanding the risk factors for dementia and developing effective preventative or therapeutic strategies for this devastating condition.