PERFORM

Scientific Program

Below is the conference itinerary. Please note that changes may be made up until the day of the conference.


07:45 - 08:30 Registration and light breakfast Foyer of Oscar Peterson Hall
08:30 - 08:35 Opening of conference,   Dr. Louis Bherer, Scientific Director, PERFORM Centre
Welcome remarks,   Dr. Graham Carr, VP Research and Graduate Studies
Session 1 Chair: Dr. Jason Steffener
Opening remarks
08:40 - 09:25 Yaakov Stern, Columbia University College of Physicians and Surgeons (includes 15 min. Q&A)
“Brain and Cognitive Reserve”  

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.

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Oscar Peterson Hall
09:25 - 10:10 Michelle Carlson, Johns Hopkins University (includes 15 min. Q&A)
“Older Adult Volunteering as a Path toward Healthy Aging: Findings from Baltimore Experience Corps Trial”  

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).

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Oscar Peterson Hall
10:10 - 10:50 Coffee break for all registrants and viewing of scientific posters *
and
Scientific poster competition: student presentations and judging
Loyola Chapel
Session 2
10:50 - 10:55
Chair: Dr. Thien Thanh Dang-Vu
Opening remarks
10:55 - 11:40 Eus J.W. Van Someren, Netherlands Institute for Neuroscience of the Royal Academy of Arts and Sciences (includes 15 min. Q&A)
“Causes and consequences of fragmented sleep in chronic insomnia”  

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.

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Oscar Peterson Hall
11:40 - 12:25 Kristen Knutson, University of Chicago (includes 15 min. Q&A)
“Impact of inadequate sleep on metabolism: a review of experimental and observational evidence”  

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.

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Oscar Peterson Hall
12:25 - 12:30 Provost's address,   Dr. Benoit Bacon Oscar Peterson Hall
12:30 - 13:55 Lunch for all registrants and viewing of scientific posters *
and
Scientific poster competition: student presentations and judging
Loyola Chapel
Session 3
13:55 - 14:00
Chair: Dr. Sylvia Santosa
Opening remarks
14:00 - 14:45 Deborah Gustafson, State University of New York-Downstate Medical Center (includes 15 min. Q&A)
“Adiposity, Metabolic Factors and Brain Health”  

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.

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Oscar Peterson Hall
14:45 - 15:30 Michael Jensen, Mayo College of Medicine (includes 15 min. Q&A)
“The Pathophysiology of Obesity and its Related Disorders”  

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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Oscar Peterson Hall
15:30 - 16:00 Round table discussion
Open floor for additional questions with all speakers.
Oscar Peterson Hall
16:00 - 16:30 Presentation of the Ed Whitlock Award & PERFORM post-doctoral fellows
Presentation of Scientific Poster Competition Awards
Closing remarks
Oscar Peterson Hall
16:30 - 17:30 Refreshments Foyer of Oscar Peterson Hall

* Optional tour of PERFORM available during the breaks. Signup required the morning of the event.

Note: all presentations will be in English.







Questions? Contact us at performcentre@concordia.ca


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