PERFORM

Invited Speakers

We are very pleased to welcome a distinguished group of international speakers to this inaugural event, representing a variety of disciplines relating to physical activity and brain functions.


Yaakov Stern, Ph.D.   [show bio]

Professor of Neuropsychology,
Departments of Neurology and Psychiatry

Columbia University College of Physicians and Surgeons, USA

Taub Institute for the Research on Alzheimer’s Disease and the Aging Brain

Yaakov Stern is Professor of Neuropsychology in the Departments of Neurology and Psychiatry, as well as the Taub Institute for the Research on Alzheimer’s Disease and the Aging Brain, at Columbia University College of Physicians and Surgeons. Dr. Stern is chief of the Cognitive Neuroscience Division of the Department of Neurology and directs the post-doctoral training program “Neuropsychology and Cognition in Aging.”

Dr. Stern earned his B.A. in Psychology at Touro College, and his Ph.D. at the Experimental Cognition program of City University of New York.

Dr. Stern’s research focuses on cognition in normal aging and in diseases of aging, particularly Alzheimer’s disease. One strong focus of his current research program is investigating the neural basis of cognitive reserve. This concept addresses the observation that some individuals show more cognitive deficit than others in the face of brain insult. He is also conducting a large scale imaging study to identify unique neural networks underlying the major cognitive abilities affected by aging. In addition he is directing cognitive intervention studies in healthy individuals, and a natural history study of Alzheimer's disease. Dr. Stern’s research approach includes classic neuropsychological and cognitive experimental techniques, with a strong focus on functional imaging. He has published over 450 peer-reviewed papers, numerous chapters, and edited a book on cognitive reserve.


Topic: Brain and Cognitive Reserve
[show abstract]

Epidemiologic evidence indicates that lifestyle factors including educational and occupational attainment, engaging in leisure and social activities, as well as IQ are all associated with reduced risk of developing dementia. Some of these lifestyle factors have also been associated with reduced rate of cognitive decline in normal aging as well. The cognitive reserve hypothesis has been put forward to explain these findings, and posits that individual differences in the flexibility and adaptability of brain networks underlying cognitive function may allow some people to cope better with age- or dementia-related brain changes than others. Recent evidence also supports the concept of brain reserve, where anatomic changes to the brain can occur on the basis of experience and also provide reserve against age- and dementia-related pathologies. A complementary concept to cognitive or brain reserve is that of brain maintenance, which posits that specific genetic and lifestyle factors may help preserve a healthy brain. This talk will review the epidemiologic evidence for brain and cognitive reserve, and describe our efforts to use brain imaging approaches to understand the neural basis for reserve.



Michelle Carlson, Ph.D.   [show bio]

Associate Professor,
Center on Aging and Health

Johns Hopkins University, USA

Dr. Carlson leads observational and randomized, controlled trial research to evaluate both environmental and pharmacologic preventive interventions of cognitive decline and dementia risk. She serves as Johns Hopkins site PI of the national Cardiovascular Health Study (CHS).

Dr. Carlson has 10 years of experience in leading large-scale clinical trials, having served as the PI of the Johns Hopkins site of the Ginkgo Evaluation of Memory (GEMS) randomized, controlled trial (RCT), and as leader of a Project on the P01-funded Baltimore Experience Corps Trial (BECT) evaluating the impact of high-intensity volunteer service on older adults’ cognitive, brain, and physical functions. Within this randomized, controlled trial, Dr. Carlson conducted a nested Brain Health Study (BHS) to evaluate the mechanisms through which Experience Corps impacts older adults’ health using neuroimaging biomarkers, and accelerometry.

Dr. Carlson is using wearable devices to objectively link patterns of lifestyle activity to cognitive and brain health. Through this work, Dr. Carlson seeks to define how socially and cognitively enriching activity in daily life helps to buffer the brain and delay dementias of aging, particularly in underserved populations at elevated risk for health disparities.


Topic: Older Adult Volunteering as a Path toward Healthy Aging: Findings from Baltimore Experience Corps Trial
[show abstract]

The Baltimore Experience Corps Trial (BECT) was designed to evaluate the impact of 2 years of volunteer service in Baltimore City elementary schools on older adults’ health and children’s academic success. The nested Brain Health Study (BHS) further evaluated Experience Corps’ impact on objectively measured physical activity and on brain biomarkers. We hypothesized that generative engagement through high-intensity community service in Experience Corps (EC) over 2 years would lead to increases in lifestyle activity and improvements in cognitive, psychological and physical health. Over 2 years, we observed modest intervention-related benefits in feelings of generativity, rates of cognitive and social activity, in objectively measured daily physical activity, and in total cortical and hippocampal volumes. Furthermore, findings in men and women suggest that differences in the magnitude of intervention-related changes may be related to baseline differences in levels of activity (less active v. more active). Given these encouraging results from a real-world intervention conducted in a group at elevated risk for disease by virtue of education, income, and minority status, we are now expanding upon our objective assessment of daily physical activity. We will describe methods we are developing to identify whether EC participation led to long-term maintenance of daily physical and lifestyle activities using standard performance (in clinic) and wearable sensors to capture the full range of benefits that are proposed to lead to a compression of risk for costly diseases of aging (dementia, frailty, disability).



Eus J.W. Van Someren, Ph.D.   [show bio]

Head of the Department Sleep and Cognition

Netherlands Institute for Neuroscience of the Royal Academy of Arts and Sciences

Professor of Neurophysiology

VU University, Amsterdam, Netherlands

Eus J.W. Van Someren was trained in physics, psychophysiology and neuropsychology and received a cum laude PhD in neurobiology from the faculty of medicine. He is Head of the Department Sleep and Cognition at the Netherlands Institute for Neuroscience of the Royal Academy of Arts and Sciences and is professor of Neurophysiology at the VU University, Amsterdam. He received prestigious grants including the NWO-VIDI and VICI. His ±200 peer-reviewed publications in scientific journals including NJEM, Jama, Nature Neuroscience, Archives of General Psychiatry, Psychological Bulletin and PNAS have been widely cited (H-index 41).

His expertise covers sleep, circadian rhythms, cognition, aging, thermoregulation, imaging and acquisition and analysis of physiological and behavioral time-series. He recently founded a Sleep Registry (www.sleepregistry.eu) to obtain a database of sleep phenotypes of many volunteers that can donate subjective and performance data every once in a while through internet. He is co-founder of the European Insomnia Network and member of the Insomnia Genetics Consortium. These are all large-scale efforts to accelerate progress in the understanding of risk factors, genetic predispositions and brain mechanisms involved in sleep and its disturbances.

His informal and easy manner and infectious enthusiasm for sleep and cognitive neuroscience make him a frequently invited speaker for lay, neuroscience and medical audiences and include an internet-broadcasted TED-X lecture.


Topic: Causes and consequences of fragmented sleep in chronic insomnia
[show abstract]

Insomnia is the most common health complaint in elderly people and has severe consequences. It is characterized by subjective sleep complaints and objective sleep fragmentation. Our understanding of underlying brain mechanisms is limited. Age-related changes in the circadian circuit fragment the sleep-wake rhythm (PNAS 2009;106:2490), which in turn contributes to age-related changes in brain function (Nat Neurosci 2009;12:122) and cognition (J Sleep Res 2009;18:129). Fragmented sleep-wake rhythms are associated with depression, obesity and (Chronobiol Int 2013;30:1223). Support of the clock by means of bright light slightly improves the sleep-wake rhythm amplitude, mood and daytime function (JAMA 2008;299:2642).

However, heterogeneity of causes of insomnia is likely. For example, MRI DTI showed that individuals with a lower axial diffusivity of white matter have less pronounced spindles and slow waves – sleep events known to guard the brain from waking up (J Neurosci 2013;33:227). MRI VBM showed that individuals with a lower gray matter volume in the mid-posterior orbitofrontal and anterior insular cortex are more prone to wake up early (Front Neurol 2012;3:105). The same cortical region shows less gray matter volume in people with insomnia (Biol Psychiatry 2010;67:182; Sleep 2013;36:999) and is implicated in hedonic evaluation. Indeed, insomniacs show a deficiency in experiencing comfort (Sleep 2008;31:1301). Moreover, people with insomnia show insufficient recruitment of the head of the caudate nucleus (Brain 2014;137:610), a structure that is strongly innervated by the orbitofrontal cortex and implicated in the regulation of cortical excitability, which deviates in insomniacs as well (Biol Psychiatry 2010;68:950). In summary, these findings start to reveal a vulnerable circuit involved in insomnia complaints that has no known role in circadian regulation.

Still, neither the circadian circuit nor the orbitofrontal-caudate circuit are necessarily involved in insomnia. E.g. in people with depression, the neural correlate of insomnia severity rather involves the thalamus. Thus, there are many reasons to lie awake. We may need to determine subtypes in large samples (Front Neurosci 2009;3:436). To start doing so we asked the help of thousands of volunteers to fill out a large number of web-surveys. Poor sleepers and good sleepers alike, because the latter carry the secret we need to know to help insomniacs (www.sleepregistry.org). Preliminary Latent Class Analyses indeed indicate different subtypes of insomnia.



Kristen Knutson, Ph.D.   [show bio]

Assistant Professor,
Department of Medicine, Section of Pulmonary and Critical Care

University of Chicago, USA

Sleep, Metabolism and Health Center

University of Chicago, USA

Kristen Knutson received her PhD in biomedical anthropology from the University at Albany, SUNY and was a postdoctoral scholar in the Section of Endocrinology, Diabetes and Metabolism at the University of Chicago. Currently, she is an Assistant Professor in the Department of Medicine, Section of Pulmonary and Critical Care at the University of Chicago. She is also a member of the Sleep, Metabolism and Health Center.

As a biomedical anthropologist, she is interested in how sociocultural factors intersect with sleep physiology to impact human health. Her research focuses on the association between sleep and cardiometabolic health, including obesity, diabetes and cardiovascular disease. Her previous research included analyzing sleep and health among nationally representative study of adolescents in the U.S. (the National Longitudinal Study of Adolescent Health) as well as an epidemiologic study of sleep (CARDIA), a diabetes survey study, a cross-cultural study, and a study of sleep in Haiti.

Moving forward, her research will examine whether sleep partially mediates socioeconomic and/or racial/ethnic disparities in cardiometabolic diseases and whether intervention to improve sleep could help to improve cardiometabolic function.


Topic: Impact of inadequate sleep on metabolism: a review of experimental and observational evidence
[show abstract]

It is well-recognized that rates of obesity and diabetes are increasing rapidly world-wide and that we need to identify modifiable causes of both diabetes and obesity in order to develop novel interventions. Although changes in diet and exercise play an important role, another possible risk factor for diabetes and obesity is reduced sleep duration and quality. This presentation will explore both the experimental and epidemiological evidence for an association between metabolic diseases and sleep duration and quality. Potential pathways leading from insufficient or disturbed sleep to diabetes and obesity will be presented and include impaired glucose metabolism, increases in appetite, differences in dietary behavior, and changes in immune function.



Deborah R. Gustafson, Ph.D.   [show bio]

Professor,
Department of Neurology, Section for NeuroEpidemiology

State University of New York-Downstate Medical Center

Adjunct , Neuropsychiatric Epidemiology Research Unit

University of Gothenburg, Sweden

Deborah Gustafson is a Professor at the State University of New York-Downstate Medical Center, Department of Neurology, Section for NeuroEpidemiology. She is Adjunct at the University of Gothenburg, Neuropsychiatric Epidemiology Research Unit, in Sweden. Dr. Gustafson was the first to report on a relationship between overweight and risk of Alzheimer's disease based on population studies in Sweden. She continues to explore potential mechanisms of adipose tissue, as well as vascular and metabolic factors, in relationship to mental disorders and brain structure in epidemiologic studies of those with conditions that may predispose them to aging-related mental disorders.

She has a global research focus and collaborates with research teams in Europe and South America. In New York City, she is Co-PI of the Women’s Interagency HIV Study (WIHS), a multi-center cohort study in the US. In these studies, she is exploring aging in HIV as well as the role of overweight and obesity, adipose tissue hormones, and genetic susceptibility in relation to a variety of outcomes including: cognition, dementia and AD, and depression. Deborah is the recipient of grants from the National Institutes of Health (NIH, USA), the European Union, and the Swedish Research Council. Dr. Gustafson has over 100 peer-reviewed or invited publications. She is an invited speaker at international meetings on the topics of adiposity, vascular factors, and prevention of dementia and other mental disorders in the elderly. Deborah received her educational training from the University of Minnesota and held an NIH postdoctoral fellowship.


Topic: Adiposity, Metabolic Factors and Brain Health
[show abstract]

Each year, obesity or obesity-related conditions lead to the deaths of 2.8 million adults around the world (World Health Organization). Due to the ageing global population, Alzheimer’s disease (AD) and dementia are also burgeoning concerns. Being overweight or obese, as measured with body mass index (BMI) or central adiposity (waist circumference), as well as evolving trajectory of BMI over the life course, have been associated with risk of all-cause late-onset dementia and AD, as well as underlying pathologies such as brain atrophy, white matter changes, and decreased blood brain barrier integrity. This observation leads us to question what it is about obesity that is associated with health of the brain and dementia risk. If high BMI and central adiposity represent more adipose tissue, the largest endocrine organ, then the endocrine aspect of adipose tissue, mediated by adipose tissue hormones and adipokines, may be a clue to understanding the association with dementia and AD. Hundreds of hormones, peptides and cytokines, which are collectively referred to as adipokines, have been identified, creating a complexity that is challenging to simplify. These adipokines affect processes in the periphery and the central nervous system. Thus, adipokines are being investigated in association with clinical dementia outcomes, as well as imaging-based measures of brain volume, structure and function in preclinical and human models of clinical dementia. Obesity is a pandemic and a serious global health concern, resulting in increased health costs and millions of deaths each year. Even diseases of latest life, such as dementia, are affected.



Michael D. Jensen, M.D.   [show bio]

Professor of Medicine,
Director of the Department of Medicine Obesity Treatment Research Program

Tomas J. Watson, Jr. Professorship in Honor of Dr. Robert L. Frye

Mayo College of Medicine, Rochester, MN, USA

Michael D. Jensen, M.D. holds the Tomas J. Watson, Jr. Professorship in Honor of Dr. Robert L. Frye at the Mayo College of Medicine, Rochester, MN. He is the Director of the Department of Medicine Obesity Treatment Research Program at Mayo Clinic. His clinical interests are primarily focused on obesity and diabetes. Dr. Jensen's research involves the study of obesity, body fat distribution, and fatty acid/energy metabolism, focusing specifically on the effects obesity and body-fat distribution on health and on the determinants of body fat distribution.

His studies have identified the relative contributions of different fat depots to lipid fuel metabolism, including the role of intra-abdominal fat. He received a MERIT award from NIH to continue his studies in this area and has been funded for 26 consecutive years. He has served on NIH, Mayo and foundation scientific review panels and has contributed to professional associations both by committee work and in elected office. Dr. Jensen has published more than 220 original research articles, together with over 50 invited papers and book chapters. He is served as co-chair of the NHLBI Expert Panel on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults.


Topic: The Pathophysiology of Obesity and its Related Disorders
[show abstract]

A primary role of adipose tissue is to store fatty acids as triglycerides when fuel supply exceeds demand and to release free fatty acids when fuel demands exceed supplies. Normal functioning adipose tissue is highly responsive to insulin’s antilipolytic effects, which in turn enhances the ability of insulin to stimulate glucose uptake, storage and oxidation. Failure to suppress lipolysis results in simultaneous elevations of glucose, insulin and free fatty acids. Chronic exposure to this environment creates what has been referred to as “lipotoxicity”. It is believed that the elevated fatty acids are shunted to signaling molecules, including diacylglycerols and ceramides that in turn reduce insulin action. One of the best predictors of dysregulated adipose tissue lipolysis is a central body fat distribution with excess visceral fat. However, visceral fat contributes only a minor fraction of systemic plasma free fatty acids. Visceral fat probably is more important in affecting hepatic function.





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