Day 1 :
Keynote Forum
Robert J Brent
Fordham University, USA
Keynote: Cost-benefit analysis of dementia interventions
Time : 11:20-12:05
Biography:
Robert J Brent is currently working as a Professor in the Department of Economics at Fordham University, New York. Previously, he was an Associate Professor in the Department of Economics at Fordham University. His research interests are Health, Development and Public Economics, etc.
Abstract:
Cost-benefit analysis (CBA) is the way to ascertain whether any kind of health care intervention is to be judged socially worthwhile. A worthwhile intervention is one where the benefits (the outcomes of everyone affected valued in monetary terms), exceeds the costs, also valued in monetary terms. Since the costs of interventions are reasonably well understood, the main challenge for CBA is to obtain a method for estimating the benefits that recognizes the reality of the scarcity of economic resources, yet also incorporates principles of fairness and justice. In this talk, a number of different benefit methods will be presented. Each method will be applied to a particular dementia intervention that has been evaluated using CBA. The expectation is that there will be at least one benefit method that someone would feel comfortable adopting for use in the CBA of any dementia intervention. There will be four main dementia CBAs presented: years of education, Medicare eligibility, hearing aids, and corrective lenses (glasses). All four dementia CBAs relied on a very large US panel data set provided by the National Alzheimer’s Coordination Center (NACC). The main strengths and weaknesses of the data will be explained. The instrument that is used to measure dementia in this data set is the Clinical Dementia Rating (CDR) scale, which covers six main domains: memory, orientation, judgment and problem solving, community affairs, home and hobbies, and personal care. The advantages of using the CDR, which focuses on dementia symptoms (cognitive functioning) rather than dementia brain pathology (plaques, fibers, etc.) are then highlighted. The talk will conclude by showing how the four CBA interventions, that focus on dementia symptoms, are complementary with efforts in Europe and the US that seek to evaluate dementia rehabilitation also on the basis of dementia behavior, especially TAP (the Tailored Activity Program).
Keynote Forum
Romeo Vitelli
Private Practitioner, Canada
Keynote: When is a head injury more than a head injury? TBI and dementia in seniors
Time : 10:15-11:00
Biography:
Romeo Vitelli, C. Psych., is a registered psychologist in the Province of Ontario with areas of competence in clinical neuropsychology and forensic psychology. He received his doctorate from York University in 1987 and has been a registered psychologist since 1988. Along with being an active blogger with the Huffington Post and Psychology Today, he is also the author of three books and is a member in good standing of the International Neuropsychological Society and clinical neuropsychology divisions of "The Canadian and American Psychological Associations".
Abstract:
Though traumatic brain injury (TBI) has been widely recognized as a leading cause of death and disability around the world, there is still considerable controversy about the potential role it plays in the development of later cognitive, including Alzheimer's disease (AD). Despite this controversy, research has shown that even a single moderate to severe head injury can lead to increased amyloid-beta (A) plaques and neurofibrillary tangles, two of the hallmark signs of AD. Also, a recent study looking at autopsy-confirmed dementia cases found that a substantial percentage of recorded cases have a prior history of head injury. In particular, older adults reporting a moderate to severe head injury involving loss of consciousness began showing symptoms of dementia three years earlier than participants with no history of TBI. Even when controlling for other factors such as lifetime history of depression, family history of dementia, level of education, and medical history, the link between dementia and TBI remains strong. Though more research is needed to explore the TBI-dementia link, health care and legal professionals need to be aware of the increased risk faced by older adults recovering even from accidents that may not be considered serious by objective standards.This includes the often thorny problem of proving causality in dementia cases arising from injuries sustained in slip and fall cases, automobile accidents, elder abuse, and other instances involving mild to moderate concussion. A recent case study will be presented to help demonstrate the legal and medical ramifications of dementia symptoms in a head-injured older senior.
Keynote Forum
Panteleimon Giannakopoulos
University Hospitals of Geneva, Switzerland
Keynote: Amyloid deposition in brain aging: Causal agent or innocuous bystander?
Time : 11:55 AM- 12:35 PM
Biography:
Professor P. Giannakopoulos completed his medical studies at the University of Athens where he graduated in 1988. His psychiatric training was performed clinically in London (Maudsley Hospital) Geneva and Paris. He is a professor and department head in department of the Geneva University Hospitals of psychiatry since 1998. Promoted to full professor in 2004, he is head of the department of psychiatry hospital and assistant dean in charge of postgraduate education in the faculty of medicine. Since 2006, he serves on the executive committee and the board of directors of the HUG (University Hospitals of Geneva). In 2008, he received the distinction of Commander of the Order of the Phoenix in his country of origin.
Abstract:
PET amyloid imaging has been initially considered as the main tool to investigate the beginning of the AD process in cognitively intact individuals. The percentage of PET-amyloid positive controls is of 6% at age 60 but reaches 50% at age 90 in community-based sample pointing to the fact that amyloid deposition (as amyloid plaque formation) is closely related to aging process. In fact, increased PiB binding has been reported in almost 20%-30% of cognitively preserved elders mainly in posterior cingulate cortex, precuneus and prefrontal cortex. Compared with amyloid-negative, amyloid-positive controls showed moderate decline in verbal and visual episodic memory over 36 months but no changes in non-memory functions. Most importantly, the absence of amyloid in MCI cases is associated with cognitive stability at 36 months. Increased PET-PiB binding is associated with brain atrophy, cortical thinning but also decreased cortical metabolism, aberrant functional connectivity at rest and decreased task-related deactivation of the default mode network. Altogether these data suggest that contrasting with CSF Aß and tau changes that sign a biological diathesis to neurodegeneration, amyloid positivity in the human brain is present as a part of the aging process representing a critical step preceding the installation of AD pathophysiology. However, not all cases with elevated PET-PiB bindings evolve to AD and several cases develop dementia not necessarily related to amyloid aggregation.Several recent contributions revealed that neurodegeneration takes place without a temporal link with fibrillar amyloid deposits. Alternative but less frequent pathways exist starting from tau deposition with modest Aß pathology.