The 2024 Doctoral Anne Martin-Matthews Prize of Excellence in Research on Aging
Each year, the Canadian Institutes of Health Research-Institute of Aging (CIHR-IA) recognizes the highest ranked doctoral trainee in the field of aging from the CIHR open doctoral competition as the CIHR-IA Anne Martin-Matthews Prize of Excellence in Research on Aging recipient.
Recipient
Tetiana Poliakova, University of British Columbia
Tetiana Poliakova is a third-year PhD student and a Vanier scholar in the graduate program of neuroscience at the University of British Columbia in Vancouver supervised by Dr. Cheryl Wellington. Tetiana's PhD project aims to increase the translational value of Alzheimer's disease mouse models by reconstituting cholesteryl ester transfer protein (CETP) expression in mice to "humanize" their peripheral lipoprotein profile. Tetiana has an excellent academic and research record at world-leading universities, including a master's degree in biomedicine from Karolinska Institutet in Sweden. Motivated by her interest in advancing translational research in dementia, Tetiana seeks to understand how we can develop more relevant animal models to design better therapeutics for Alzheimer's disease. In addition to her graduate studies, Tetiana is the chair of the International Student Acceleration and Advising Committee in the Graduate Program of Neuroscience and the co-founder and director on the Ukrainian non-profit, English2Doctors.
Disorders in fat, or lipid, metabolism are now recognized to play a key role in brain disorders including Alzheimer's Disease (AD), the most common type of dementia. Previously, most studies focused on the roles of brain lipids in the development of dementia, and, despite knowing that circulating lipids affect dementia risk, the contributions of blood lipids to AD have largely been ignored. Specifically, in humans, elevated levels of low-density lipoprotein (LDL), also known as “bad” cholesterol, are associated with a higher risk of AD. Humans typically have 70-80% of their total cholesterol in LDL and the other 20-30% in high-density lipoprotein (HDL), or “good” cholesterol. Oppositely, mice, which are frequently used in animal models of AD to study AD development and test therapies, have 80% of their circulating cholesterol in HDL. This prevents us from effectively studying how circulating lipids contribute to the development of AD. The reason why mouse “good” to “bad” cholesterol ratio is different from humans is that mice are naturally deficient in cholesteryl ester transfer protein (CETP), the activity of which raises LDL and lowers HDL. My project aims to “humanize” mouse blood lipid profile by crossing transgenic mice that express CETP with established models of AD. By using techniques such as RNA sequencing and histology, we aim to understand how putting back CETP into mice affects the development and progression of amyloid plaques (one of the defining features of AD) and changes in the blood vessel network in the brain. We expect that CETP expression will worsen the hallmarks of AD in mice. If so, in the future, we can test CETP inhibitors, which are already being tested for use in cardiovascular diseases, as an effective intervention to improve AD-related outcomes.
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