Director of research and innovation, CHUM and Scientific director, CRCHUM

À confirmer.

Professor of molecular Neuroendocrinology and program leader at the MRC Metabolic Diseases Unit, University of Cambridge, UK Genetics of obesity: Can an old dog teach us new tricks? It is clear that the cause of obesity is a result of eating more than you burn. It is physics. What is more complex to answer is why some people eat more than others? Differences in our genetic make-up mean some of us are slightly more hungry all the time and so eat more than others. In contrast to the prevailing view, obesity is not a choice. People who are obese are not bad or lazy; rather, they are fighting their biology. Research Area His focus is on the study of obesity, brain control of body weight and genetic influences on appetitive behaviour

Neurologist, Montreal Neurological InstituteProfessor, Department of Neurology and Neurosurgery Mc Gill University, Canada. Obesity as a cause of neurodegenerative disease Midlife obesity is the most common modifiable risk factor for Alzheimer’s Disease (AD) and vascular dementia, and it consistently relates to poorer cognition and brain atrophy. Obesity causes a decline in brain health through hyperlipidemia, hypertension, inflammation, and insulin resistance. Brain magnetic resonance imaging (MRI) reveals that individuals with higher body mass index (BMI), even in early adulthood, exhibit a loss of grey and white matter. These midlife obesity-associated brain changes are thought to represent an early lesion that predisposes to progressive neurodegeneration and dementia. We will present evidence from large datasets such as UK Biobank and Human Connectome Project that (1) visceral adiposity leads to cortical thinning and cognitive impairment via inflammation and cerebrovascular disease (2) the pattern of cortical tissue loss resembles that seen in AD and (3) weight loss from bariatric surgery may reverse these changes. I ntroduced by: Thierry Alquier

Physician, Department of hepatology, CHUM, Principal scientist, Immunopathology theme, CRCHUM Research Area Introduced by: Sabri Ahmed Rial Obesity as a cause of neurodegenerative disease Midlife obesity is the most common modifiable risk factor for Alzheimer’s Disease (AD) and vascular dementia, and it consistently relates to poorer cognition and brain atrophy. Obesity causes a decline in brain health through hyperlipidemia, hypertension, inflammation, and insulin resistance. Brain magnetic resonance imaging (MRI) reveals that individuals with higher body mass index (BMI), even in early adulthood, exhibit a loss of grey and white matter. These midlife obesity-associated brain changes are thought to represent an early lesion that predisposes to progressive neurodegeneration and dementia. We will present evidence from large datasets such as UK Biobank and Human Connectome Project that (1) visceral adiposity leads to cortical thinning and cognitive impairment via inflammation and cerebrovascular disease (2) the pattern of cortical tissue loss resembles that seen in AD and (3) weight loss from bariatric surgery may reverse these changes.

Postdoctoral fellow, CRCHUM, Laboratory of Naglaa Shoukri, Immunopathology theme Two transcriptionally and functionally distinct waves of neutrophils during mouse acute liver injury.

Metabolic vulnerabilities in advanced breast cancer Associate Vice-President, Research Support and Infrastructure, Office of the Vice-President, Research and Innovation. Research area Her central research focus is the understanding of metabolic adaptation to physiological and pathological conditions, notably, the role of the master regulators PGC-1s in cancer, with a particular focus on poor outcome breast cancers. Introduced by: Réjean Lapointe

Principal scientific and Theme leader, Cardiometabolic research theme, CRCHUM and professor at the Department of medicine, Université de Montréal Neuronal lipid droplets in the central control of energy homeostasis This presentation will highlight the previously unrecognized role of neuronal triglyceride metabolism and lipid droplets in the regulation of whole-body energy homeostasis by hunger-activated AgRP neurons. Field of research Thierry Alquier's research investigates metabolic signaling in hypothalamic regions that regulate energy homeostasis and their contribution to obesity with a particular focus on lipid sensing and astrocyte-neuron communication.

Postdoctoral fellow, Thierry Alquier and Ciaran Murphy-Royal laboratories Glucocorticoid receptors in astrocytes : Star players in energy homeostasis

Associate Professor, Institute of Health Policy, Management and Evaluation, Toronto University and researcher at St. Michael’s Hospital in Toronto. Research area Dr. Booth’s research focuses on health outcomes related to diabetes; specifically how socioeconomic, environmental and health care factors influence the risk of diabetes and its complications. Presented by : Lise Gauvin

Professor, Cumming School of Medicine, Department of Cell Biology and AnatomyFull Member, Mathison Centre for Mental Health Research and Education, Calgary University Endocannabinoids, Cannabis and Feeding Behavior Cannabis is well known to promote food intake, a process widely known as "the Munchies". Cannabis exerts its effects on physiology and behavior through its interaction with the endocannabinoid system. The ability of endocannabinoids, and cannabis, to influence feeding behavior appears to be multifactorial and involve multiple neural processes. This talk will review the current state of knowledge regarding how endocannabinoids and cannabis interact with feeding hormones and the neural circuits and behavioral mechanisms by which they promote food intake. Introduced by: Ciaran Murphy-Royal

Principal scientist, Cancer theme, CRCHUMAssistant professor, Faculty of pharmacy, Université de Montréal Targeting the adenosine immune checkpoint in cancer: is our model correct? Senior scientist at CRCHUM and Full Professor at UdM, Dr Stagg made seminal discoveries in the field of immuno-oncology. His work notably sparked the development of therapeutics agents targeting the adenosine immune checkpoint that are now in late-stage clinical trials. In this presentation, Dr Stagg will present new data highlighting the complex mechanism of adenosine-mediated immunosuppression and discuss how adenosine transport and metabolism regulates T cell function Introduced by: Sabri Ahmed Rial

Postdoctoral fellow, John Stagg laboratory, Cancer theme The CD73 immune checkpoint promotes tumor cell metabolic fitness

Panel

Panel: 30 years since the discovery of Leptin Giles Yeo, Matthew Hill, Alain Dagher Moderator: Thierry Alquier

Closing remarks and invitation to the cocktail