2013 SPEAKER BIOS, ABSTRACTS, AND POWERPOINT PRESENTATIONS
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Ranjan Duara, MD
Speaker – Introduction
Ranjan Duara, MD, is the Medical Director of the Wien Center for Alzheimer’s Disease and Memory Disorders at Mount Sinai Medical Center in Miami Beach. He is a Professor of Neurology at the Herbert Wertheim College of Medicine (Department of Neurology) at Florida International University and is affiliated with the University of Miami, Miller School of Medicine, Miami, Florida (Depts. of Medicine, Neurology and Psychiatry). He completed internal medicine and neurology residencies in India, the United Kingdom and at Thomas Jefferson University Hospital in Philadelphia, and did a fellowship in neuroscience and neuroimaging at NIH.
Dr. Duara’s research has focused primarily on early diagnosis of Alzheimer’s disease and other dementias, neuroimaging, genetic epidemiology and the methodology for staging the transition from normal cognitive aging to dementia. He has contributed to over 200 articles in peer-review scientific journals as well many book chapters. Dr. Duara is the Principal Investigator for the State of Florida Alzheimer’s Disease Initiative Brain Bank. He has also been an investigator in numerous clinical trials of novel agents for the treatment of Alzheimer’s disease.
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Dr. Duara’s Introductory Speech at the 11th Annual MCI Symposium
David A. Bennett, MD
Speaker – Symposium
David A. Bennett, MD, is the Robert C. Borwell Professor of Neurological Sciences and director of the Rush Alzheimer’s Disease Center. Dr. Bennett received the degree of bachelor of science with high distinction and high honors in physiology from the University of Michigan, Ann Arbor, in 1979. He earned his doctorate in medicine from Rush Medical College in 1984. Following his medical internship, Dr. Bennett returned to Rush for residency training in neurology and a research fellowship in dementia. Internationally known for his research regarding the causes, treatment and prevention of Alzheimer’s disease and other common neurologic conditions of aging, Dr. Bennett’s primary research interest is understanding the neurobiologic pathways linking genetic and environmental risk factors to loss of cognition, and understanding why many older persons are able to live with severe Alzheimer’s disease changes in the brain without suffering from memory loss (cognitive or neural reserve). Dr. Bennett is principal investigator of several studies funded by the National Institute on Aging, including the Rush Alzheimer’s Disease Core Center, the Religious Orders Study and the Rush Memory and Aging Project. He also directs the Regional Alzheimers Disease Assistance Center for Northern Illinois for the Illinois Department of Public Health. He serves on numerous state, national, and international advisory and editorial boards, and has more than 300 manuscript publications.
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New Approaches to Understanding the Relationships of Risk Factors to Cognitive Decline
We used data from the Religious Orders Study and the Rush Memory and Aging Project to examine the associations between risk factors, neuropathology, and cognitive decline. The trajectory of cognitive decline can be characterized in three components: the onset of cognitive decline and the slope prior to and after the onset of decline. Risk factors for incident AD andMCI are differentially related to these three components of decline. Some risk factors change with time as does cognitive function. Cross-lagged models can be used to identify the leading indicator, i.e., whether change in the risk factor leads cognitive decline or vice versa. We can also link neuropathology to the trajectories of cognitive decline, including change point models,and investigate the pathways linking risk factors to cognitive decline. Finally, cognitive change is the result of the competing effects of pathologies which lead to cognitive decline and resilience markers which maintain cognition. We are beginning to identify these indices and incorporate them into models of cognitive decline and neuropathology.
Tammie Benzinger, MD, PhD
Chair – Mini-Symposium 2
Dr. Benzinger’s res
earch focuses on translating advanced neuromagnetic resonance imaging techniques from small animal research in the Department of Radiology, to translational research in the Center for Clinical Imaging Research (CCIR), and into clinical practice. In particular, her current research focuses on using directional diffusivity meaurements derived from diffusion tensor imaging (DTI) to measure axonal and myelin damge in pediatric and adult demyelination, dysmyelinating diseases, in traumatic brain injury (TBI) and as a function of aging. Diseases under study in Dr. Benzinger’s laboratory include Alzheimer’s disease, multiple sclerosis (MS), acute disseminated encephalomyelitis (ADEM), adrenoleukodystrophy, Krabbe’s disease, Pelizaeus-Merzbacher’s disease, and head trauma. In addition, Dr. Benzinger combines advanced neuromagnetic resonance techniques, such as DTI and spectroscopy, and positron emission tomography (PET) to study interactions between normal aging, Alzheimer’s disease, depression and delirium in older adults.
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Maria Carrillo, PhD
Panelist – Forum
Dr. Carrillo is Vice President, Medical and Scientific Affairs, at the Alzheimer’s Association. At the Association, Dr. Carrillo has a wide range of responsibilities, including oversight of the Association’s granting process and communication of scientific findings within and outside of the organization. Dr. Carrillo is responsible for overseeing the International Research Grant Program, the mechanism through which the Association funds research. In addition to ensuring the smooth review of applications and distribution of awards to successful applicants, she is responsible for sharing results and ongoing investigations with a wide range of constituents. Dr. Carrillo also manages several Association initiatives. One of these is the Alzheimer’s Association Research Roundtable, which provides a forum for pharmaceutical companies to discuss trends in Alzheimer research and therapeutic targets. Other Association programs managed by Dr. Carrillo include the management of the World-Wide Alzheimer’s Disease Neuroimaging Initiative (WW-ADNI), which is a multi-country research effort aimed at finding biomarkers for early detection of Alzheimer’s, and the Working Group on Technology (WGT), which aims to promote the use of technologies available today for the support of individuals affected by Alzheimer’s disease to retain their independence as long as possible. Dr. Carrillo is a member of the Genworth Financial Medical Advisory Board. Dr. Carrillo received her Ph.D. from Northwestern University’s Institute for Neuroscience in 1996. Since graduating from Northwestern, she completed a postdoctoral fellowship in the Division of Neurological Sciences at Rush University Medical Center in Chicago, where she later took a position as an assistant professor.
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The Importance of Being Informed and Participating in Trials
Without clinical trials, there will be no better therapy, no prevention and no cure for Alzheimer’s disease, the 6th leading cause of death in the United States. TheAlzheimer’s Association® is the largest voluntary health agency dedicated toAlzheimer’s disease and is committed to advancing research forward and engages in a number of strategies to facilitate the clinical trial enterprise and educate constituents around the importance of clinical trials. The largest barrier in development and advancement of clinical trials, however, remains the recruitment and retaining of volunteers. Alzheimer’s Association TrialMatch™ is a free service that enables consumers (individuals with Alzheimer’s disease, healthy volunteer, caregivers) and healthcare professionals to identify clinical trials in their communities based on personal search criteria. Bringing together a consortium of industries invested in the Alzheimer’s clinical trial space, the Alzheimer’s Association Research Roundtable® facilitates the development and implementation of new treatments for Alzheimer’s disease by collectively addressing obstacles to research and development, clinical care, and public health education. Examples include classification of Alzheimer’s disease, evaluation of clinical trial safety related events, and examination of factors to improve phase 2 clinical trials. The Association further addresses public health education through multiple avenues: our national chapter network, on-going communication and web releases, and educational workshops (e.g. Know the 10 Signs about the early warning signs ofAlzheimer’s disease); physician outreach to help information and provide resources to physicians across the US.
Bradford C. Dickerson, MD, MMSC
Speaker – Symposium
Dr. Dickerson has
a broad background in behavioral neurology, neurodegenerative disease, neuroimaging, and cognitive neuroscience, and has been performing neuroimaging and behavioral research for more than 15 years. In addition to basic systems-level neuroscientific research on memory, social function, emotion, and aging, Dr. Dickerson has developed an approach to the use of novel imaging and behavioral measures as markers for use as diagnostics and monitoring of neurodegenerative diseases. He is currently Director of the MGH Frontotemporal Dementia Unit and the Dickerson Neuroimaging Laboratory and Co-Director of the Imaging Subcore of the Alzheimer’s Disease Research Center.
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The Cortical Signatures of Alzheimer’s Disease and Frontotemporal Degeneration: Quantitative MRI Biomarkers Detectable Prior to Dementia
One hallmark of neurodegenerative diseases is the selective degeneration of specific brain regions. In Alzheimer’s disease (AD) and Frontotemporal Dementia (FTD), specific regions of the cerebral cortex develop neurodegenerative pathology early in the course of the diseases. A variety of neuroimaging techniques are capable of detecting abnormalities in brain structure and function, which can provide in vivo evidence suggestive of specific neuropathologies. In routine clinical evaluation, the visualization of atrophy on magnetic resonance imaging (MRI) in specific sets of brain regions can provide support for the diagnosis of one of the neurodegenerative dementias. However, early in the course of many of these diseases, atrophy may be subtle.Quantitative measurements from MRI can provide further information supportive of specific diagnoses. In this talk I will discuss our work on the identification of the “cortical signatures” of AD and FTD dementia—the cortical regions that are consistently atrophic in patients with mild forms of these neurodegenerative dementias. I will highlight our recent work using these signature measures in an a priori fashion to try to more confidently detect subtle atrophy in the pre-dementia and preclinical stages of these illnesses.At the conclusion of this presentation, the attendees should be able to 1) explain how MRI can be used to measure the size of specific brain regions; 2) describe how these measurements can be used in research and clinical practice in dementia and mild cognitive impairment; and 3) discuss the potential future uses of these measurements in clinical research and trials of putative interventions.
Anne Fagan, PhD
Speaker – Workshop
Anne M. Fagan, Ph
D, is a Research Professor of Neurology at Washington University School of Medicine in St. Louis. Anne is a faculty member in The Knight Alzheimer’s Disease Research Center and the Hope Center for Neurological Disorders and serves as the Biomarker Core Leader for several longitudinal studies investigating the diagnostic and prognostic utility of fluid measures as biomarkers of preclinical and early clinical AD pathology in elderly and middle-aged cohorts. She is also the Biomarker Core Leader for the observational DIAN study of families harboring autosomal-dominant AD gene mutations, and the secondary prevention trial in such affected families (DIAN Trial Unit; DIAN-TU). In addition to her work characterizing fluid biomarker profiles in the preclinical and early stages of AD, Anne has been actively involved in world-wide biomarker protocol development, validation, and standardization efforts, issues that are critical to address in order to move fluid biomarkers forward into clinical practice.
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The Role of Fluid Biomarkers in Preclinical Alzheimer’s Treatment Trials
Clinicopathologic and biomarker studies of Alzheimer’s disease (AD) support the notion of a long asymptomatic (“preclinical”) stage of the disease, with brain pathology (Beta-amyloid plaques and neurofibrillary tangles) estimated to begin ~10-15 years prior to significant neuronal cell death and the appearance of behavioral signs or symptoms of dementia. Cerebrospinal fluid (CSF) levels of A-Beta1-42 and tau (and phosphorylated tau species), markers of Beta-amyloid plaques and neurofibrillary tangles/neurodegeneration, respectively, have together shown prognostic utility for predicting cognitive decline (within 3-5 years) in cognitively normal older individuals, development of future dementia in cohorts with Mild Cognitive Impairment (MCI) and the rate of cognitive decline in individuals diagnosed with very mild dementia. Fluid biomarkers are now being considered in the design of treatment as well as prevention trials, as outcome measures and for subject enrollment. Three secondary prevention trials in asymptomatic/preclinical cohorts are currently in development (DIAN TU, API, A4). Although similar in concept and approach, they differ in the disease-modifying treatments being tested, the criteria for subject enrollment, and the specific biomarker measures for enrollment, target engagement and/or outcomes. At the conclusion of this presentation the attendees should be able to: 1) explain what is known about the diagnostic and prognostic utility of fluid biomarkers in the preclinical period, 2) describe the three prevention trials currently being developed, and 3) discuss the strengths and challenges of the use of fluid biomarkers in such trials.
Adam S. Fleisher, MD, MAS
Speaker – Workshop
Adam S. Fleisher, 
MD, MAS, currently serves as the Director of Imaging at Banner Alzheimer’s Institute. He is also an Associate Professor, Department of Neurosciences, at the University of California, San Diego (UCSD), where he is the Medical Director of the Alzheimer’s Disease Cooperative Study. Dr. Fleisher received his medical degree from the University of Rochester School of Medicine, New York, and obtained his general neurology training at Johns Hopkins Hospital in Baltimore, Maryland. He then completed a clinical and research dementia fellowship at UCSD, as well as a Master’s degree of advanced studies in clinical research. He is a practicing dementia neurologist, clinical trialist and imaging researcher. He is well published in both MRI and PET imaging, as well as clinical trials in Alzheimer’s disease, with a research focus on influences of aging and genetic risk factors for Alzheimer’s disease and predictive biomarker development in cognitively normal elderly adults.
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The Role of Amyloid Imaging in Preclinical Alzheimer’s Treatment Trials
Amyloid imaging continues to play a prominent role in understanding the pathology of Alzheimer’s disease, development of predictive tools for dementia, and clinical treatment trials. This year we will see the launch of three asymptomatic anti-amyloid treatment trials: 1) the Dominantly Inherited Alzheimer’s network treatment trial, 2) the Alzheimer’s Prevention Initiative anti-amyloid antibody trial, and 3) the Anti-Amyloid treatment of Asymptomatic Alzheimer’s disease (A4) trial. Amyloid imaging has played a critical role in the development of these trials, and will be important for monitoring of drug pharmacodynamics and relation to clinical outcome measures during the trials. At the conclusion of this presentation the attendees should be able to 1) Explain the relevance of amyloid imaging in the study of asymptomatic individuals at risk for Alzheimer’s disease, 2) Describe how amyloid imaging is being used in current asymptomatic Alzheimer’s disease trials, and 3) Discuss future opportunities for the role of amyloid imaging in clinical trial research.
Mary Ganguli, MD, MPH
Chair/Speaker – Mini-Symposium 1
Dr. Mary Ganguli, MD, MPH, is Professor of Psychiatry, Neurology, and Epidemiology at the University of Pittsburgh School of Medicine and Graduate School of Public Health. She is also a clinically active board-certified geriatric psychiatrist on the medical staff of the University of Pittsburgh Medical Center. Dr. Ganguli has been continuously funded since 1986 by the National Institute on Aging (NIH) to conduct epidemiologic studies of cognitive impairment and dementia within population-based cohorts (www.wpic.pitt.edu/research/dementia_epidemiology). Dr. Ganguli has served on the National Advisory Council on Aging, on several NIH study sections, on the DSM-5 work group on neurocognitive disorders (American Psychiatric Association), on practice parameter work groups on mild cognitive impairment (American Academy of Neurology), as associate editor or editorial board member on several journals.
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Risk Factors for MCI Development and for MCI Progression: Are they the Same?
Mild cognitive impairment (MCI) is a state intermediate between normal cognition and dementia. At the population level, MCI is more heterogeneous than in the clinical research setting where most research is conducted, and heterogeneity with regard to outcomes most likely reflects etiological heterogeneity. Vascular disease is an established risk factor for dementia. In a large prospective population-based cohort, we examined a range of vascular/metabolic/ inflammatory factors in relation to risk both of incidence of new-onset MCI and of progression from MCI to dementia, using both cognitive and functional (Clinical Dementia Rating) definitions. Some similar and some different vascular risk and protective factors were found for incidence and for progression. These findings confirm that vascular disease and risk factors are also risk factor for MCI and dementia, but also suggest that some factors sufficient to lead to mild impairment may not be sufficient to influence further progression to dementia. Identifying at-risk individuals to control their vascular morbidity has potential for both lowering risk of MCI and also risk of progression to dementia at the population level.
Todd Golde, MD, PhD
Keynote Lecturer – Symposium
Dr. Golde is professor of Neuroscience at the University of Florida (UF) and the Director of UF’s Center for Translational Research in Neurodegenerative Disease. Dr. Golde has made significant contributions to the Alzheimer’s disease (AD) field. During his studies as an MD PhD student he played a pivotal role in pioneering studies showing that genetic causes of AD alter production of a normal protein called Aβ in a way that leads to its aggregation and accumulation in the brain. These studies provided crucial support for the A aggregation hypothesis of Alzheimer’s disease and enabled drug discovery programs aimed at altering A production and deposition. Based on these studies and similar work form other groups, virtually every major pharmaceutical company developed programs to find inhibitors of Aβ production.
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Solving the Dilemma of Treatment Versus Prevention Strategies for Alzheimer’s Disease
Effective therapy for Alzheimer’s disease (AD) is a major unmet medical need. Based on estimates that ~35 million people worldwide have AD today, well over 120 million individuals may have AD in 2050. If nothing is done the toll of the AD epidemic will be enormous. Although key aspects of AD pathogenesis remain enigmatic, scientific advances made over the last three decades have provided sound rationale for the development of potentially disease-modifying therapies. These therapies primarily target the suspected trigger or triggers of the disease. Therapies that have advanced the farthest have primarily been developed based on the proposed initiating role of amyloid b-protein (Ab) aggregates. These therapeutic advances coupled with advances in early detection of AD-related pathology in non-demented individuals, suggest that concerted translational research efforts focusing on prevention or early intervention could dramatically reduce the incidence and prevalence of AD. This assertion is supported by preclinical studies showing that anti-Aβ therapies may be highly effective if tested as agents to prevent or delay development of the disease or as therapies for asymptomatic patients with very early signs of AD pathology. However, until the recent launch of several early intervention trials in genetically at risk populations, anti-Aβ therapeutics have been tested in symptomatic patients where they are likely to be much less effective. Although there has been recent movement towards earlier intervention trials, there are still many scientific and non-scientific obstacles to translating preclinical and diagnostic advances into successful prophylactic therapies. Continuing recognition and open discussion of these obstacles by the scientific community, policy makers and others with vested interests in more effectively combating AD is needed in order to further develop road maps that address and eventually overcome the obstacles to developing effective disease modifying AD therapies.
Hugh Hendrie, MB, ChB, DSc
Speaker – Symposium
Dr. Hugh Hend
rie, MB, ChB, DSc, is currently a professor with the Department of Psychiatry, Indiana University School of Medicine and a center scientist with the IU Center for Aging Research. His research has been primarily in clinical epidemiology involving international comparative studies in dementia and cognitive decline as well as in intervention studies for the treatment of late life depression and dementia in medical clinics.
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The Fluidity of MCI and the Role of Vascular Biomarkers in Predicting Progression Results from the Indianapolis-Ibadan Study
Hendrie HC, Gao S, Lane K.A and members of the Indianapolis-Ibadan dementia project
Mild Cognitive Impairment (MCI) has been considered to be an early stage of dementia. However previous studies have suggested that MCI is also heterogeneous disorder with many with MCI reverting to normal. The transient status of MCI is explored in an analysis of data from the Indianapolis-Ibadan dementia project. The analysis included 3982 elderly African American participants studied for up to 17 years. In this analysis the transition from normal cognition to MCI occurred significantly more frequently than normal to dementia (age standardized annual transition rates normal to MCI 5.6%, normal to dementia 0.7%). Both MCI transition to normal and to dementia were also common (age standardized transition rates MCI to normal 18.6% and MCI to dementia 5.9%) with MCI transition to dementia being significantly more common with increasing age. In 2001 measurements of cardiovascular biomarkers were added to the study. However an analysis of cohorts of elderly African Americans and Yoruba with MCI indicated that the addition of these single measurements did not add significantly to predictions of MCI to Dementia transitions. Survival analysis in the African American and Yoruba cohorts suggested that the diagnosis of MCI added an increase in mortality risk of a similar magnitude for both populations.
Jason Karlawish, MD
Speaker – Workshop
Jason Karlawish is a Professor of Medicine, Medical Ethics and Health Policy at the University of Pennsylvania. He is the Associate Director of the Penn Memory Center and the Director of the Alzheimers Disease Center’s Education, Recruitment and Retention Core. His research focuses on neuroethics, particularly as it related to research and care of older adults, and persons with neurodegenerative diseases such as Alzheimers Disease and Parkinsons Disease. His has investigated issues in dementia drug development, informed consent, quality of life, research and treatment decision making, biomarkers, and voting by persons with cognitive impairment and residents of long term care facilities. He developed the ACED – the assessment for capacity for everyday decision making — an instrument to assist in judging a person’s capacity to manage their functional deficits. His current research is examining the clinical and policy implications of how risk is changing concepts of disease, medicine, health and aging. This work has introduced the concept of “desktop medicine,” a model of medicine grounded in a concept of disease as risk and treatment as risk reduction.
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Addressing the Ethical Challenges of Preclinical AD Prevention Trials for the Early Alzheimers Disease Workshop
To move the concept of pre-clinical AD from a provocative idea to a target of clinical care, researchers need to perform clinical trials. These studies will provide essential criterion validation that links biomarker or genetic measures to valuable clinical outcomes, but the design and conduct of these trials present interrelated scientific and ethical challenges. These include:
1. Whether and, if so, how, to disclose biomarker or genetic status to participants.
2. Monitoring subject safety.
3. The impact of knowing biomarker and genetic status on cognitive self efficacy and performance.
4. The impact of study participation on employment and insurance.
This presentation will discuss these challenges with attention to summarizing the range of options to address them, their tradeoffs, and what research could help to address them. At the conclusion of this presentation the attendees should be able to (1) explain the ethical challenges of pre-clinical AD trials, (2) describe strategies and studies needed to address them, and (3) discuss the policy challenges presented by pre-clinical AD trials.
Susan M. Landau, PhD
Speaker – Forum
Dr. Susan Landau is Research Neuroscientist at the Helen Wills Neuroscience Institute at the University of California, Berkeley and the Lawrence Berkeley National Laboratory. Her research focuses on the longitudinal evaluation of multiple biomarkers in aging, mild cognitive impairment, and Alzheimer’s disease. Recent work with the Alzheimer’s Disease Neuroimaging Initiative (ADNI) has examined the predictive role of amyloid PET imaging, and other genetic, cerebrospinal fluid, and imaging biomarkers in cognitive decline at different phases of disease. Other recent work has examined the role of cognitive activity and lifestyle factors in aging and amyloid deposition, and the impact of chemotherapy on neural and cognitive function.
Dr. Landau studied cognitive psychology and neuroscience at Wesleyan University and completed a PhD at UC Berkeley, where she also received a National Science Foundation Graduate Research Fellowship award. She has carried out research on learning, working memory, and dopamine in healthy aging and dementia using PET and functional MRI. She has received additional training in cognitive neuroscience and neuroimaging at Dartmouth University, in neuropsychological evaluation at the Memory and Aging Center at the University of California San Francisco, and in electrophysiology at the Center for the Neural Basis of Behavior at the University of Pittsburgh.
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Evaluation of Different Biomarkers Ability to Predict Cognitive Decline at Various Stages of Alzheimer’s Disease
Susan M. Landau PhD, Helen Wills Neuroscience Institute, University of California, Berkeley, Lawrence Berkeley National Laboratory
As amyloid PET imaging becomes more prevalent, a key question is to determine when its predictive value is greatest, and how amyloid measurements relate to other biomarkers across different phases of disease. We have evaluated several biomarkers and their relationship to longitudinal cognitive decline in participants from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) population. Different biomarkers appear to be valuable in predicting decline and progression at different phases of disease. Specifically, associations between amyloid and cognitive function are frequently stronger in the earliest phases of disease (asymptomatic amyloid+ normal individuals), while in MCI, hypometabolism may be more directly linked than amyloid to cognitive decline. These findings support a model in which amyloid deposition is associated with the earliest stages of subtle cognitive impairment, followed by neuronal injury that parallels further cognitive decline and disease progression. Integrating information from multiple biomarkers longitudinally will be critical for identifying which individuals decline and which remain stable over time.
Allan Levey, MD, PhD
Speaker – Forum
Allan Levey, MD, P
hD is a professor and chair of the Department of Neurology at Emory University’s School of Medicine, as well as the director of Emory’s Alzheimer’s Disease Research Center. He has secondary faculty appointments in the Departments of Pharmacology, Psychiatry and Behavioral Sciences. Levey is an internationally recognized expert in neurodegenerative disorders. His work has contributed to understanding the brain systems and mechanisms involved in disorders such as Alzheimer’s and Parkinson’s diseases, as well as in identifying molecular targets for new therapeutic strategies. He has more than 250 research publications and has won several awards, including the Derek Denny-Brown Neurological Scholar Award from the American Neurological Association, the Heikkila Research Scholar Award from the National Parkinson Foundation, the Health Advancement Research Award from Community Health Charities and the Team Hope Award for Medical Leadership from the Huntington’s Disease Society of America. In addition, he was inducted into the Johns Hopkins Society of Scholars.
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John Morris, MD
Speaker – Workshop / Panelist – Forum
John C. Morris
, M.D. is a leading researcher in the fight against Alzheimer’s disease. Dr. Morris is the Harvey A. and Dorismae Hacker Friedman Distinguished Professor of Neurology, Professor of Pathology and Immunology, Professor of Physical Therapy, and Professor of Occupational Therapy at Washington University. He also is the Director and Principal Investigator of the Charles F. and Joanne Knight Alzheimer’s Disease Research Center at Washington University School of Medicine. Dr. Morris is a member of the Alzheimer’s Association’s Medical & Scientific Advisory Committee. He chairs the Clinical Task Force for the NIA’s Alzheimer Disease Centers program. He is author or co-author of over 400 peer-reviewed journal articles and 50 chapters and reviews. He edited the first and second editions of the Handbook of Dementing Illnesses. He has received many honors, including the Distinguished Achievement Citation from his alma mater, Ohio Wesleyan University (2000), the Lifetime Achievement Award from the Alzheimer’s Association (2004), the 2004 MetLife Foundation Award for Medical Research, the 2005 Potamkin Prize for Research in Pick’s, Alzheimer’s, and Related Disease from the American Academy of Neurology and the Physician-Scientist Lifetime Achievement Award (2005) and the 2006 Dr. Neville Grant Award for Clinical Excellence from the Barnes-Jewish Hospital Foundation (St. Louis, MO). In 2008, he received the Washington University Academic Women’s Network Mentor Award. In 2010, he received the Carl and Gerti Cori Faculty Achievement Award from Washington University. He is ranked in the top 1% of investigators in the field of Neuroscience and Behavior by Essential Science Indicators database.
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A New Era: DIAN and The Secondary Prevention of Symptomatic Alzheimer’s Disease
JC Morris, MD on behalf of the DIAN investigators, Knight Alzheimer’s Disease Research Center, Washington University, Saint Louis, MO
Given the failure of putative “disease-modifying” drugs to date to benefit individuals with symptomatic Alzheimer disease (AD), it is time to consider the potential efficacy of these agents when administered in the preclinical (asymptomatic) stage of the illness, prior to the irreversible loss of synaptic and neuronal integrity.Establishing a cohort of participants who are members of families with a known mutation (PSEN1, PSEN2, APP) causing autosomal dominant AD (ADAD) is ideal for “Secondary prevention” trials, as asymptomatic mutation carriers (MCs) are at ~100% risk of developing symptomatic AD at a predictable age (Based on the affected parent’s age at onset). Hence, the Dominantly Inherited Alzheimer’s Network (DIAN) was established in 2008 to develop and characterize such a cohort. The initial recruitment goal of 240 people for the international DIAN performance sites already has been exceeded, as by November 1, 2012, 302 participants had completed baselines assessments; recruitment of new participants to the cohort continues as does as emphasis on longitudinal follow-up assessments. Most importantly, the DIAN Trials Unit will launch within months simultaneous trials in MCs of three agents with the initial goal of demonstrating target engagement and the ultimate goal of delaying or even preventing cognitive decline.
Ronald C. Petersen, MD, PhD
Speaker – Symposium
Ronald C. Petersen, MD, PhD, is the Cora Kanow Professorship in Alzheimer’s Disease Research, and a Mayo Clinic Distinguished Investigator at the Mayo Clinic. He is on the National Advisory Council on Aging, and is the chair of the Advisory Council on Research, Care and Services for the National Alzheimer’s Project Act by the Secretary of the Department of Health and Human Services. Dr. Petersen is the recipient of the 2004 MetLife Award for Medical Research in Alzheimer’s Disease, and the 2005 Potamkin Prize for Research in Pick’s, Alzheimer’s and Related Disorders of the American Academy of Neurology.
Peter V. Rabins, MD, MPH
Speaker – Symposium
Peter V. Rabins the
inaugural Richman Family Professor of Alzheimer’s and Related Diseases, was born in Everett, Massachusetts, and raised in Hollywood, Florida. After graduating from the University of Florida, he received MD and MPH degrees from Tulane University in New Orleans. He then completed a one-year internship in internal medicine at Tulane and a psychiatry residency at the University of Oregon Health Sciences Center (now the Oregon Health and Sciences University). Dr. Rabins came to Johns Hopkins in 1977 to do a one-year fellowship with Marshal Folstein in consultation/neuro-psychiatry and was appointed as an assistant professor and the founder of the Geriatric Psychiatry Program in 1978. He has been a professor of psychiatry since 1993 and serves as vice chair for academic affairs in the psychiatry department. He has joint appointments in the departments of Health Policy and Management and Mental Health in the Johns Hopkins Bloomberg School of Public Health, and is a member of the Johns Hopkins Berman Institute of Bioethics. Early in his career Dr. Rabins (along with Folstein) was the first to demonstrate that delirium predicted increased mortality in the year after discharge from hospital, a finding that has since been widely replicated. In the same year he published the earliest paper establishing the high prevalence of psychiatric symptoms in patients with dementia and demonstrated that these symptoms correlate with distress in family caregivers (JAMA 1982). In 1981 Dr. Rabins co-authored, with Nancy Mace, The 36-Hour Day. This book remains the best-selling family guide to the care of people with Alzheimer’s disease and other dementias, selling over 2.25 million copies to date, and its four editions have sold more copies than any other book published by the Johns Hopkins Press. In recent years Dr. Rabins has focused his research on improving the delivery of psychiatric care to the elderly and on the study of the non-Alzheimer dementias. He developed and demonstrated the efficacy of a nurse-centered model of care to elders living in public housing (JAMA 2000) that has been certified as one of the few evidence-based practices in geriatric psychiatry. He has developed scales to measure quality of life and severe cognitive impairment in dementia, and has led a team studying the care of patients with late-stage dementia. With David Blass he described a new form of fronto-temporal dementia (Neurology, 2004) and with Brian Appleby has identified several new clinical presentations of Creutzfeldt-Jakob disease.
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Correlates of Conversion to Dementia in a Prospective Community-Ascertained Cohort
Rabins, PV, Lyketsos, CG, Corcoran C, Tschanz, J.
Almost 100% of individuals have plaques and tangles in their brain if they survive to age 90. This suggests that the development of dementia due to AD may be inevitable and strategies to delay onset (secondary prevention) deserve more attention. This presentation identifies correlates of age of onset identified in a community-ascertained cohort followed for 12 years.
Eric Reiman, MD
Speaker – Workshop / Panelist – Forum
Dr. Reiman is Exe
cutive Director of the Banner Alzheimer’s Institute (BAI), Chief Executive Officer for Banner Research, Clinical Director of the Neurogenomics Division at the Translational Genomics Research Institute (TGen), Professor of Psychiatry at the University of Arizona, and Director of the Arizona Alzheimer’s Consortium. His research interests include brain imaging, genomics, and their use in the unusually early detection and tracking of Alzheimer’s disease (AD), the evaluation of genetic and non-genetic risk factors, and the accelerated evaluation of preclinical AD treatments. He is the author of more than 200 publications, and the principal investigator of several NIH research grants, including the NIA-sponsored Arizona AD Center. He and his colleagues have used imaging techniques to detect and track some of the earliest brain changes associated with the predisposition to AD in cognitively normal people at different levels of genetic risk; they have suggested strategies and endpoints for the accelerated evaluation of preclinical AD treatments, and they established API to help find effective treatments as quickly as possible. API’s trial in ADAD mutation carriers is expected to begin in the second quarter of 2013.
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Rosebud O. Roberts, MS, MB, CHB
Speaker – Symposium
Dr. Rosebud Roberts is a Professor of Epidemiology in the Division of Epidemiology, Department of Health Sciences Research at the College of Medicine, Mayo Clinic, Rochester. She is the study epidemiologist for the Mayo Clinic Study of Aging, a National Institutes of Health funded study of approximately 3,500 persons aged 70 years and older resident in Olmsted County, Minnesota. Dr. Roberts’s research is focused on the study of normal aging, mild cognitive impairment, and dementia. Her primary research is directed towards identifying modifiable risk factors for mild cognitive impairment, with a focus on the role of key vascular risk factors such as type 2 diabetes. She has authored several peer-reviewed manuscripts on risk factors for mild cognitive impairment.
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Scott Roberts, PhD
Speaker – Workshop
Scott Roberts, PhD, is Associate Professor of Health Behavior & Health Education at the University of Michigan’s School of Public Health (U-M SPH). He completed his doctoral training in clinical psychology, with postdoctoral specialization in clinical geropsychology. From 2001-06, he was on the faculty at Boston University School of Medicine, based primarily at its NIH-funded Alzheimer’s Disease Center, where he served as Co-Director of its Education Core. During this time Dr. Roberts served as a support group leader and conducted evaluations of an Alzheimer’s Association sponsored education and support program for early-stage Alzheimer’s disease (AD). Dr. Roberts conducts research on several topics related to Alzheimer’s disease. He has published numerous articles that address participants’ motivations and interests in genetic testing, the psychological impact of providing risk disclosure, and health behavior changes prompted by risk assessment. He has also published numerous articles on attitudes, beliefs and knowledge about AD and MCI, including surveys of family members, neurologists, and the general public. Dr. Roberts has served since 2001 as Co-Principal Investigator on the NIH-funded REVEAL Study (Risk Evaluation and Education for Alzheimer’s Disease), a series of randomized clinical trials examining the impact of APOE testing for people at risk for clinical AD. In the current fourth trial, the REVEAL team has developed and is evaluating an education and risk communication protocol for individuals with mild cognitive impairment (MCI).
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Consent for Revealing Biomarker Status in AD Prevention Trials
Techniques such as genetic testing, amyloid imaging, and cerebrospinal fluid assays are viewed as critical tools for future risk assessment and tracking of disease progression in Alzheimer’s disease. However, their integration into intervention trials with preclinical populations raises numerous ethical and practical questions. What is the best way to communicate this often complex, ambiguous information? What are the likely psychosocial harms and benefits of learning one’s risk status? This session will describe both ongoing and proposed interventions in which biomarker information is disclosed to populations at “imminent” risk (i.e., within the next few years) of developing clinically expressed AD. First, findings will be presented from a series of multi-site randomized clinical trials known as the REVEAL (Risk Evaluation and Education for Alzheimer’s Disease) Study. In the current fourth trial, APOE genotype status is being disclosed to individuals with mild cognitive impairment (MCI) and their study partners. Participants randomized to the study’s intervention arm receive a genetic testing and education protocol that includes risk information based on the participant’s age, MCI status, and APOE genotype. Here, quantitative risk estimates for AD risk within the next three years (range: 8-57%) are communicated to persons with MCI aged 70 and above and their study partners (typically a spouse or adult child), along with information about education and support resources. Participants in the control arm also receive education and AD risk estimates (range: 25-44%) but without the incorporation of genetic test results. Data will be presented on study outcomes including participants’ comprehension of risk information, psychological distress, and behavior changes (e.g., advance planning) prompted by test results. The implications of study findings for practice and policy will be discussed, including the planned use of biomarkers in forthcoming AD prevention trials. The disclosure of biomarker information with uncertain clinical implications in clinically normal older individuals raises important research ethics issues regarding informed consent and determination of study risks versus social benefits. The author’s experience with the REVEAL Study will inform a consideration of the challenges and opportunities posed by disclosure of AD biomarker information in this context.
Simona Sacuiu, PhD
Speaker – Symposium
Simona Sacuiu is at University of Gothenburg in Sweden since 2001. Her research focuses on prodromal cognitive signs of dementia in population studies, and has so far resulted in eight original articles. Dr Sacuiu received her PhD at the Sahlgrenska Academy, University of Gothenburg in 2009 with a thesis on prodromal cognitive signs of dementia. During 2010 she was a short-term scholar at the Department of Radiology, Center for Imaging of Neurodegenerative Diseases, University of California, San Francisco where she initiated a study of validity of clinical neuroimaging investigation together with psychometric examination to predict dementia onset in large population studies. She also received in 2001 an MA in Psychology/ Neuroscience at the University of Delaware, USA, where she studied the response of the aging rodent brain to systemic inflammation from physiological and behavioural perspectives. Dr. Sacuiu has a medical degree from the University of Medicine in Bucharest, Romania. Currently she is a last year medical resident in Psychiatry at the Sahlgrenska University Hospital in Gothenburg, Sweden.
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The Flynn Effect; how Secular Changes Influence the Predictive Value of Cognitive Performance and the Role of Computer Tomography in Prodromal Dementia in the H70 Study in Gothenburg, Sweden
Simona Sacuiu, Boo Johansson, Erin Bigler, Ingmar Skoog
Few studies have examined whether prodromal cognitive signs of dementia are consistent across cohorts. Moreover, the role of conventional computer tomography (CT) in detecting structural brain changes in prodromal dementia is unclear. Thus, we investigated (1) cognitive predictors of dementia between 70-75 years in two cohorts born 30 years apart and (2) the association of subjective cognitive symptoms with brain atrophy and white matter lesions (WMLs) according to CT in the preclinical stage of dementia. Methods: A representative sample of 382 non-demented 70-year-olds born 1901-02 was examined regularly for dementia outcome, with the first follow-up at age 75. Cognitive assessments consisted of psychiatric and psychometric examinations. Identical examinations were conducted in another representative sample of 512 non-demented 70-year-olds born 1930 at age 70 and 75 years. Furthermore, the cohort born 1901-02 underwent brain CT at age 85 years (n=132) and was examined using self-reported symptoms. This sample was followed until death for the outcome of dementia (n=42). Brain atrophy and WMLs were classified using visual rating scales. Results: Low performance in non-amnestic psychometric tests at age 70 predicted dementia between age 71-75 years in the cohort born 1901-02, while in the cohort born 1930 there was no relation between non-amnestic psychometric tests results and incident dementia. However, memory problems at age 70 according to the psychiatric examination predicted dementia in both cohorts. In the second study of the cohort born 1901-02, participants age 85 were more likely to report low executive performance in the presence of WMLs, independently of mood disorders and self-reported memory problems. Self-reported memory problems were not associated with brain changes. The risk of incident dementia increased in those with WMLs and self- reported low executive function. At the conclusion of this presentation the attendees should be able to 1) explain why later born generations may display a compression of early signs of dementia closer to the clinical diagnosis, except memory disturbance which remains an early detectable symptom and is consistent across generations; 2) describe the differences in prodromal cognitive signs of dementia across generations of elderly ; and 3) discuss the validity of standardized psychometric testing and CT-brain scans in the work-up of cognitive impairments in primary care.
Steven Salloway, MD, MS
Speaker – Symposium
Stephen Salloway,
MD, MS, is Director of Neurology and the Memory and Aging Program at Butler Hospital in Providence, Rhode Island, and Professor of Clinical Neurosciences and Psychiatry at Brown Medical School. He is the Director of the Brown Combined Residency in Neurology and Psychiatry and Codirector of the National Institute on Aging-sponsored Brown Dementia Research Fellowship Program. He received his MD from Stanford Medical School and completed residencies in neurology and psychiatry at Yale University. Dr. Salloway has published more than 185 scientific articles, book chapters, and abstracts and has edited 3 books. His research focuses on the following areas: clinical trials for the prevention and treatment of Alzheimer’s disease, mild cognitive impairment, and vascular dementia; studies of genetic and sporadic forms of microvascular brain disease; studies of executive function and frontal behaviors; and the development of imaging biomarkers to study conversion to dementia. Dr. Salloway has received numerous grants for his research from the National Institutes of Health and from private foundations. He published the first controlled clinical trials of cholinesterase inhibitors for the treatment of mild cognitive impairment and vascular dementia. Under his direction, the Butler Memory and Aging Program has become a nationally recognized clinical research center that tests new disease-modifying treatments for Alzheimer’s disease, including amyloid vaccines, gamma secretase inhibitors and modulators, antifibrillization agents, and RAGE inhibitors. His program has also become a key research center in the United States for the study of CADASIL, a genetic disorder that causes stroke and vascular dementia.
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Highlights of Biomarker and Clinical Outcomes from Recent Alzheimer’s Disease Treatment Trials
Stephen Salloway
The results of key clinical and biomarker findings from two large multi-center trials of anti-amyloid monoclonal antibodies (bapineuzumab and solanezumab) for mild-moderate Alzheimer’s disease (AD) have important implications for the design of future AD clinical trials. The primary outcomes were negative for both compounds, the rate of decline increased with disease stage, and mild patients showed a small cognitive benefit with solanezumab on secondary analyses of the ADAS-Cog. 93% of ApoE4 carriers, but only 63-67% of non-carriers, met designated amyloid PET cut-offs. Treatment with bapineuzumab was associated with a significant difference on amyloid PET in ApoE4 carriers and in pooled analyses. However, these differences were lower than those reported in the phase 2 trials of bapineuzumab and gantanerumab. Though elevations were seen in plasma and CSF total Aβ42 with solanezumab, no difference was seen on amyloid PET. Mild significant lowering of CSF phospho-tau, a putative marker of neurodegeneration, was seen in most analyses with bapineuzumab, but not with solanezumab. A small increased rate of cortical atrophy and ventricular enlargement was seen in pooled analyses with bapineuzumab but not with solanezumab. Low rates of ARIA-E (0.5-1.1%) were seen in the placebo groups. The rate of ARIA-E was significantly higher with bapineuzumab and increased with dose and ApoE carrier status. A slightly higher rate of ARIA-E was seen with solanezumab (1% vs. 0.5%).
These findings raise important issues and questions for the design of future trials with anti-amyloid treatments. Is a biomarker effect required to see a clinical benefit? Was the biomarker effect with bapineuzumab insufficient to produce a clinical benefit? What is the mechanism of action of solanezumab? The dose of bapineuzumab was limited by symptomatic ARIA-E but there may be room to increase the dose of solanezumab. What is the clinical impact of a mild cognitive change only in patients with mild AD? Is the stage of mild-moderate dementia too advanced for these drugs to exert a major clinical benefit? Will anti-amyloid therapies be more efficacious at milder stages and what effect size might we see? Combination therapies may be required for maximizing clinical benefits. The underlying diagnosis and rate of decline in amyloid-negative subjects is unclear. Future trials in mild-moderate AD should include amyloid cut-offs on CSF or PET, especially in ApoE4 non-carriers, to ensure that study populations have AD. Uncertainty about the direction of change on volumetric MRI with anti-amyloid treatment impacts the use of vMRI in calculating sample size. The mechanism underlying increased rate of atrophy with some anti-amyloid treatments requires further investigation.
Philip Scheltens, MD, PhD
Speaker – Symposium / Discussant – Forum
Dr. Philip Scheltens studied at the VU University Amsterdam, Netherlands, gaining his MD in 1984, and PhD (Magnetic Resonance Imaging in Alzheimer’s disease) in 1993. Clinical residencies in neurosurgery at the Municipal Hospital Slotervaart, and at the VU University Medical Centre, Amsterdam, supported his academic development. Dr Scheltens is Professor of Cognitive Neurology and Director of the Alzheimer Center at the VU University Medical Center in Amsterdam. His main clinical and research interests are Alzheimer’s disease, vascular dementia, frontotemporal dementia, magnetic resonance imaging, PET imaging and biomarkers. He is active in the field of biomarkers and clinical trials and has been the national PI for many studies, including fase 1-3 multicenter clinical trials. He founded and directs the Alzheimer Center since 2000, from which over 34 PhD theses have appeared since then.
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MRI, FDG – PET and EEG for Predicting Progression in Aging, MCI and AD
Philip Scheltens, MD, PhD, VU University Medical Center, Amsterdam, Netherlands
Alzheimer’s disease (AD) is diagnosed by a combination of clinical history, signs and symptoms, and advanced imaging techniques. In the past, neuroimaging tended only to be used to exclude other causes of dementia but, increasingly, it is now also being used to distinguish between dementia types. Magnetic resonance imaging (MRI) is a particularly valuable tool in this respect, due to its ability to identify the fine detail of cerebral pathology that is specific to AD. Indeed, the new proposed research diagnostic criteria for AD include a core clinical part (subjective and objective memory disturbance) alongside biomarkers (structural MR, PET, and CSF support criteria).
Following a diagnosis of MCI, recognized as being a prodromal stage of AD in many, but not all, patients, the assessment of progression to AD is traditionally made using various psychometric tests, such as the Mini-Mental State Examination (MMSE), the Global Deterioration Scale (GDS), and the Alzheimer Disease assessment Scale Cognitive (ADAS-COG). According to the IWG and NIA-AA criteria, prodromal AD or MCI due to AD, respectively, may be identified by using biomarkers such as MRI, PET (amyloid, FDG), and CSF.
Recently the ISTAART professional interest neuroimaging group reviewed the diagnostic accuracy (likelihood ratios, LRs) of imaging biomarkers (amyloid imaging, 18F-FDG PET, SPECT, medial temporal atrophy on MRI) to separate AD from healthy and MCI converting to AD from non-converters. Accuracy was studied separately by “metrics” (i.e. how the marker is measured; e.g. manual segmentation, automated tool, etc). LR+ ranged from 9.4 to 4.4 and LR- from 0.08 to 0.25 for amyloid imaging and MRI, respectively. Prognostic LR+ ranged from 7.5 to 1.7 and LR- from 0.50 to 0.11 for 18F-FDG PET and amyloid imaging, respectively. Within individual metrics, LRs varied up to 100-fold (i.e. from 1 to 100 and from 0.01 to 1.00). Markers accounted for 11% and 18% of LR+ (diagnostic and prognostic) and for 24% and 16% of LR- variance. Across all markers, metrics accounted for an equal or larger amount of variance than markers: 13% of LR+ and 29% of LR diagnostic, and 62% of LR+ and 18% of LR- prognostic variance. Within individual markers, the largest proportion of diagnostic LR+ variability 1 was between 18F-FDG PET metrics, while the largest proportion of LR- variability was between MRI metrics. We concluded that accuracy of imaging biomarkers for AD is at least as dependent on how the biomarker is measured as the biomarker type itself.
The development of standard operating procedures for biomarker measurement will be key to biomarker use in the clinical routine. In a recent study using ADNI data the combination of MR imaging, FDG PET, and CSF data with routine clinical tests significantly increased the accuracy of predicting conversion to AD compared with clinical testing alone. The misclassification rate decreased from 41.3% to 28.4% (P < .00001). FDG PET contributed more information to routine tests (P < .00001) than CSF (P = .32) or MR imaging (P = .08). As for EEG, we recently studied associations between visual EEG findings and diagnoses in 1,116 consecutive patients [382 Alzheimer’s disease (AD), 274 subjective complaints, 190 mild cognitive impairment (MCI), 118 psychiatric disorder, 61 frontotemporal lobar degeneration, 53 vascular dementia (VaD), 38 dementia with Lewy bodies (DLB)] were determined by prevalence ratio (PR). Diagnoses of subjective complaints [PR = 1.6; 95% confidence interval (CI) = 1.4–1.9] and psychiatric disorder (1.4; 95% CI = 1.1–1.9) were associated with a normal EEG, while subjects with both focal and diffuse EEG disturbances were more likely to have DLB (3.5; 95% CI = 2.1–5.6), VaD (2.3; 95% CI = 1.4–3.6) or AD (1.5; 95% CI = 1.3–1.8). Subjects with only diffuse EEG abnormalities were more likely to have AD (PR = 1.5; 95% CI = 1.3–1.9). The prevalence of MCI was higher among those with only focal EEG abnormalities (PR = 1.3; 95% CI = 1.0–1.7). From our data we concluded that focal abnormalities on EEG as the only phenomenon may support an MCI diagnosis, while more diffuse abnormalities argue for AD or progression to AD in MCI. More recent studies focus on the use of EEG as a measure of brain connectivity studying brain networks in different disease stages.
Reisa Sperling, MD
Speaker – Forum
Reisa Sperli![Sperling-Headshot[1]](https://mcisymposium.org/wp-content/uploads/2014/10/Sperling-Headshot1-e1412217217928.jpeg)
ng, M.D. is a Professor in Neurology at Harvard Medical School and the Director of the Center for Alzheimer Research and Treatment at Brigham and Women’s Hospital. She is the Principal Investigator on the National Institute on Aging (NIA) Program Project funded Harvard Aging Brain Study and the Director of the Alzheimer’s Disease Neuroimaging Program at Massachusetts General Hospital. She served as the Chair of the NIA-AA working group to develop the criteria for “Preclinical Alzheimer’s disease”. Dr. Sperling is actively working on clinical trials of potential disease-modifying therapies in MCI and AD dementia, and will serve as the Project Leader for the ADCS Anti-Amyloid in Asymptomatic AD – the “A4” secondary prevention trial.
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Dr. Sperling’s Workshop Lecture
Prashanthi Vemuri, PhD
Speaker – Symposium
Dr. Vemuri is an Assistant Professor at the Aging and Dementia Imaging Laboratory, Department of Radiology, Mayo Clinic Rochester. She has a Masters and Doctorate from the Department of Electrical Engineering at University of Utah, Salt Lake City with a major in Medical Imaging. She completed a fellowship with Dr. Clifford Jack at the Mayo Clinic in imaging of neurodegenerative diseases. She is a recipient of the NIH/NIA K99/R00 Pathway to Independence grant award and Alzheimer Association New Investigator grant award and was recently awarded the AFAR-GE healthcare junior investigator award for excellence in aging and imaging research.Dr. Vemuri’s area of research is in developing and validating biomarkers to improve the understanding and management of Alzheimer’s disease and related disorders.
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Biomarkers, Cognitive Reserve and Cognition in Alzheimer’s Disease
In this talk, we will discuss how biomarkers can be used for prediction of future progression of Alzheimer’s Disease and for evaluating disease progression. We will present results based on MRI and CSF data from ADNI. In addition, we will discuss how cognitive reserve affects the relationship between biomarkers of Alzheimer’s disease (AD) pathophysiology and cognition. We investigated this question in two independent studies – ADNI and Mayo Clinic Study of Aging (MCSA) which is a population based cohort. In both studies we found that cognitive reserve variables (measured using verbal IQ in ADNI and lifestyle variables in MCSA) were not associated with AD biomarkers but they explained variability in the cognitive performance. These studies provide evidence that cognitive reserve may delay the onset of dementia but does not significantly influence the expression of AD pathophysiology and indicate that it is important to account for individual differences in cognitive reserve in AD studies.
Victor Villemagne, MD
Speaker – Symposium
After graduating Cum Laude in Medicine in 1983, Dr. Villemagne continued his post-graduate studies at the Division of Nuclear Medicine at the Johns Hopkins Medical Institutions. Dr. Villemagne subsequently furthered his functional neuroimaging research at the National Institute on Drug Abuse, NIH, and at the University of Pittsburgh, before joining the Melbourne Neurodegeneration team in 2003. He has over a 100 publications in international peer-reviewed journals on PET research, particularly in the field of neuroscience and neuroreceptor studies. He has been invited to chair and present at national and international meetings in the area of biomarkers for Alzheimer’s disease and neurodegeneration. In 2001, he received the Foerderer Fund for Excellence Award from The Children’s Hospital of Philadelphia in the USA, the ANSTO Neuroscience Nuclear Medicine Award, and in 2007 the JAAME Fellowship from the Ministry of Health and Labor in Japan. Currently, Dr. Villemagne is CI in several NHMRC project grants, a NEDO grant from Japan and an ADDF grant from the USA involving Ab and tau imaging and the characterization of new blood borne Alzheimer’s disease biomarkers.