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Ranjan Duara, MD

Speaker – Introduction

duara_headshotRanjan 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 12th Annual MCI Symposium

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Tammie Benzinger, MD, PhD

Speaker – Forum

headshot_benzingerDr. Benzinger’s research 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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Dr. Benzinger’s Workshop Lecture

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When Amyloid Imaging Isn’t Enough

Tammie Benzinger, Nupur Ghoshal, Washington University School of Medicine, St. Louis, MO, USA


A 73-year-old woman presented for routine serial research MRI and amyloid Pittsburgh Compound B (PiB)PET (1) imaging as part of a longitudinal study of memory and aging at Washington University (NIH/NIA P01AG026276, PI: J. Morris).  The case is presented from the perspective of the radiologist, who was called upon to assess her when she had difficultly answering questions for the Mini Mental Status Examination (MMSE)(2).  Longitudinal volumetric MRI scans processed with FreeSurfer(3) for hippocampal volumes, cortical thickness regions suspected in Alzheimer’s disease (AD) (4) and in primary progressive aphasia(5, 6) were analyzed and compared with cerebrospinal fluid (CSF) biomarkers(7) and clinical assessments including the Clinical Dementia Rating (CDR) (8).  Resting state functional connectivity MRI (rs-fcMRI) was used to localize language areas (9, 10).


1.         Morris JC, Roe CM, Grant EA, Head D, Storandt M, Goate AM, Fagan AM, Holtzman DM, Mintun MA. Pittsburgh compound B imaging and prediction of progression from cognitive normality to symptomatic Alzheimer disease. Arch Neurol. 2009;66(12):1469-75. Epub 2009/12/17. doi: 10.1001/archneurol.2009.269. PubMed PMID: 20008650; PubMed Central PMCID: PMC2798814.

2.         Feng L, Chong MS, Lim WS, Ng TP. The Modified Mini-Mental State Examination test: normative data for Singapore Chinese older adults and its performance in detecting early cognitive impairment. Singapore medical journal. 2012;53(7):458-62. Epub 2012/07/21. PubMed PMID: 22815014.

3.         Fischl B. FreeSurfer. NeuroImage. 2012;62(2):774-81. doi: 10.1016/j.neuroimage.2012.01.021.

4.         Bakkour A, Morris JC, Dickerson BC. The cortical signature of prodromal AD: Regional thinning predicts mild AD dementia. Neurology. 2009;72(12):1048-55. doi: 10.1212/01.wnl.0000340981.97664.2f.

5.         Gorno-Tempini ML, Dronkers NF, Rankin KP, Ogar JM, Phengrasamy L, Rosen HJ, Johnson JK, Weiner MW, Miller BL. Cognition and anatomy in three variants of primary progressive aphasia. Ann Neurol. 2004;55(3):335-46. doi: 10.1002/ana.10825. PubMed PMID: 14991811; PubMed Central PMCID: PMC2362399.

6.         Grossman M. Primary progressive aphasia: clinicopathological correlations. Nature reviews Neurology. 2010;6(2):88-97. doi: 10.1038/nrneurol.2009.216. PubMed PMID: 20139998; PubMed Central PMCID: PMC3637977.

7.         Sutphen CL, Fagan AM, Holtzman DM. Progress Update: Fluid and Imaging Biomarkers in Alzheimer’s Disease. Biol Psychiatry. 2013. Epub 2013/09/10. doi: 10.1016/j.biopsych.2013.07.031. PubMed PMID: 24012326.

8.         Morris JC. The Clinical Dementia Rating (CDR): current version and scoring rules. Neurology. 1993;43(11):2412-4. PubMed PMID: 8232972.

9.         Shimony JS, Zhang D, Johnston JM, Fox MD, Roy A, Leuthardt EC. Resting-state spontaneous fluctuations in brain activity: a new paradigm for presurgical planning using fMRI. Academic radiology. 2009;16(5):578-83. doi: 10.1016/j.acra.2009.02.001. PubMed PMID: 19345899; PubMed Central PMCID: PMC2818666.

10.        Schummer G. The disconnection syndrome:; 2009 [cited 2014 1/10/2014]. Available from:

Howard M. Chertkow, MD

Chair – Workshop

Howard Cherheadshot_chertkowtkow is a cognitive neurologist, Professor of Neurology at McGill University in Montreal Canada, and he has been director of the Jewish General Hospital/ McGill University Memory Clinic for 20 years. His major areas of research interest include: 1) Early diagnosis of Alzheimer’s disease and prediction of deterioration in individuals with Mild Cognitive Impairment. 2) the structure, organization, and function of the Semantic Memory component of long term memory, and its deterioration in dementia , and 3)  localization of language and memory functions in the brain using functional imaging. Dr. Chertkow is past president of the Consortium of Canadian Centres for Clinical Cognitive Research (C5R), the national Canadian organization of clinical research on Alzheimer’s Ddisease and he is currently leading the initiative to establish a Canadian Consortium for Neurodegeneration and Aging. In 2005 his team published the Montreal Cognitive Assessment (MoCA), which has become an international standard for diagnosis of MCI. In 2006 he chaired the Third Canadian Consensus Conference on the Diagnosis and Treatment of Dementia, which brought together many of the country’s experts to formulate new guidelines for physicians. Results have been published nationally and internationally.  In 2008 Dr. Chertkow received the national Irma Parhad Award from C5R for contributions to excellence in Alzheimer’s disease research. In 2011 Dr. Chertkow was the only Canadian member of the NIH team which revised the diagnostic criteria for Alzheimer’s disease (McKhann, Knopman, Chertkow et al, 2011). Dr. Chertkow represents the Canadian Institutes of Health Research on the executive board of ADNI, the Alzheimer’s Disease Neuroimaging Initiative.

Gaël Chetelat, PhD

Speaker – Symposium

headshot_chetelatGaël Chételat is Director of Research at INSERM and Head of the research team « Multimodal neuroimaging in brain diseases » in the Inserm Unit U1077 in Caen. Mentored by Jean-Claude Baron and Francis Eustache, she obtained a PhD in neuroscience and neuropsychology in 2002 and has been working since then in the field of normal and pathological aging, especially Alzheimer’s disease, using various neuroimaging techniques. She performed a 2-year sabbatical (2009-2011) in the laboratory of Christopher Rowe in Melbourne (Australia) where she conducted studies on amyloid neuroimaging with PiB-PET. She developed specific expertise in the use of multimodal neuroimaging to better understand the pathological mechanisms of neurodegenerative diseases. She has more than 80 articles published in peer-reviewed journals and is internationally recognized for her researches in the field. She has recently been awarded by the de Leon Prize in Neuroimaging (AAIC 2012).

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Dr. Chetelat’s Mini-Symposium Lecture

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Variation in the Sequence of AD Biomarkers According to Brain Regions and Genetic Factors

Gaël Chetelat, Inserm-EPHE-Université de Caen/Basse-Normandie, Caen, France


Inspired by the amyloid cascade hypothesis, the dominant view is that, when considering AD biomarkers, amyloid deposition appears first, followed by neuronal dysfunction, and then atrophy (all preceding cognitive decline). We conducted a series of studies highlighting the variation of this chronology across brain regions. Thus, we showed that the relative degree of atrophy, hypo-metabolism and amyloid deposition greatly varies according to the brain area considered. This highlights the fact that, at least locally, there is not a single sequence of events, which in turn suggests that the underlying pathological mechanisms are both multi-determined and variable. Other evidences reinforce this view, showing that the sequence may also vary across AD cases, notably when considering sporadic late-onset AD versus early-onset mutation carriers and/or in ApoE4 carriers. Altogether, these results may change the way we consider the pathophysiology of this disease, suggesting more independent processes and/or different possible pathways.

Sara Czaja, PhD

Speaker – Symposium

headshot_czajaSara J. Czaja, PhD, is a Leonard M. Miller Professor of Psychiatry and Behavioral Sciences University of Miami Miller School of Medicine and Industrial Engineering at the University of Miami. She is also the Director of the Center for Research and Education for Aging and Technology Enhancement (CREATE) and the Scientific Director of the Center on Aging at the Miller School of Medicine. CREATE is a collaboration between the University of Miami, the Georgia Institute of Technology, and Florida State University, and it is funded by the National Institute on Aging.

Dr. Czaja has extensive experience in aging research and a long commitment to developing strategies to improve the quality of life for older adults. She is also the Director of the evaluation component of the NIH funded Miami Clinical & Translational Science Institute. Her research interests include aging and cognition, e-health, caregiving, human computer interaction, and functional assessment.  She has published extensively on these topics. She is a fellow of the American Psychological Association, the Gerontological Society of America, and the Human Factors and Ergonomics Society. Dr. Czaja served as the overall Chair of the Health Services Research and Demonstration study section for the Veterans Administration and as the Chair of the Risk Prevention and Health Behavior Review Panel for the National Institutes of Health. She is currently a member of the College of Reviewers for the NIH. She is also a member of the Board on Human Systems Integration of the National Academy of Science/National Research Council (NAS/NRC) and served as a member of the recent NAS/NRC committee on Human Factors in home healthcare.

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Dr. Czaja’s Mini-Symposium Lecture

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Computer-based Assessment of Functional Performance in MCI

Sara J. Czaja, Philip D. Harvey, David Loewenstein, University of Miami Miller School of Medicine, Miami, FL, USA


It is well recognized that people with cognitive impairments such as dementia or Mild Cognitive Impairment (MCI) often experience difficulty performing routine everyday tasks such as money or medication management that are critical to independent living. With the aging of the population, especially the increase in the “oldest old” (aged 85+), there are vast concerns about the increasing number of people who will experience cognitive problems that threaten their ability to live independently. Thus, there is an increasing interest in developing tools to both detect the earliest manifestations of cognitive and functional decline in order to prescribe remediation strategies or to measures effectiveness of treatment approaches.

Currently much of the assessment of functional performance is based on standardized neuropsychological measures of abilities, paper and pencil based tests of functional performance or informants’ assessment of performance. The shortcomings of these measures have been widely documented. Ultimately, development of efficacious strategies to optimize functional performance requires understanding the performance of on actual tasks encountered in everyday life. Technology offers a flexible format that allows for easy tailoring of the assessment protocols to meet the needs of unique populations or settings and the possibility of administering assessments and delivery interventions remotely outside of clinical settings such as the home, residential facilities or outpatient treatment centers.

This presentation will focus on an innovative approach to functional assessment, which involves ecologically valid technology-based functional assessment battery of simulations of everyday activities that are important to independent living including: using an ATM to perform banking transactions, a telephone menu system to refill prescriptions, a medication forms completion task, a shopping task and doctor’s visit/medication management task. The simulations are unique in that they present current technology-based versions of these tasks, which is important given the ubiquitous requirements for use of technology across all domains important to independent functioning. They are presented on a standard touch screen PC and available in English and Spanish. The task performance data included real time measures of accuracy, types of difficulties encountered by the participants and response times. Data will be presented from an on-going NIH funded trial that includes older adults with MCI and non-impaired older adults regarding the feasibility and diagnostic sensitivity of the computer-based task battery. Information will also be presented on the relationships between component cognitive abilities and task performance.

Charles DeCarli, MD

Speaker – Workshop

headshot_decarliCharles DeCarli, MD, is Professor of Neurology at the University of California in Davis, California and recipient of the Victor and Genevieve Orsi Chair in Alzheimer’s Research.  He is the Director of the UC Davis Alzheimer’s Disease Center, a United States National Institutes of Health funded Alzheimer’s research center.   Dr. DeCarli is also Director of the Imaging of Dementia and Aging (IDeA) laboratory. His research focuses on using advanced structural and functional brain imaging to study normal aging, mild cognitive impairment and dementia and the role of genetics, cerebrovascular and Alzheimer’s disease on these processes.  He has published over 300 peer-reviewed journal articles in high impact journals such as Brain, Lancet Neurology and Nature Genetics. Dr. Decarli is a recipient of the J. Allyn Taylor International Prize in Medicine—Imaging of the Aging Brain in recognition of his work. In addition, he is the Editor-in-Chief of Alzheimer Disease and Associated Disorders, an international journal of AD research.

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Dr. DeCarli’s Workshop Lecture

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A Case of Vascular MCI

Charles DeCarli, MD, University of California, Davis, CA, USA


Mild Cognitive Impairment is a heterogeneous disorder.  MCI is generally described as either memory or non-memory impairment followed by sub-classification by the presence or absence of impairments in additional cognitive domains.  The vast majority of individuals with the amnestic form of MCI are believed to have prodromal Alzheimer’s disease, however, amyloid imaging of this subgroup of individuals not uncommonly is negative.  Cerebrovascular disease, particularly subcortical cerebrovascular disease can present with amnestic features and a slowly progressive course consistent with prodromal Alzheimer’s disease.  This case which is presented from initial evaluation through to autopsy and includes repeated neuropsychological testing, MRI and PiB imaging, highlights features that may help guide the clinician to consider vascular cognitive impairment instead of AD.

Hiroko H. Dodge, PhD

Speaker – Symposium


Dr. Dodge joined the NIA-funded Oregon Alzheimer’s Disease Center (OADC) as the data core director in 2008. She is currently Associate Professor of Neurology at Oregon Health & Science University and Adjunct Research Associate Professor of Neurology at University of Michigan.  Before joining the OADC, she was a faculty member jointly with the Department of Epidemiology and the Department of Biostatistics at University of Pittsburgh. She is a member of the Executive Council of OADC, and a Data Core Steering Committee member for the National Alzheimer’s Coordinating Center, established by the National Institute on Aging in 1999 to facilitate collaborative research among the 29 NIA-funded Alzheimer’s Disease Centers nationwide.

Dr. Dodge’s research has been focused on three areas. One is to distinguish normal cognitive aging from pathological cognitive decline. She is refining statistical methods which allow us to capture the decline leading to dementia at the earliest stage of the disease. Another is to examine lifestyle and environmental factors leading to healthy cognitive aging. She has been conducting a cohort study in Okinawa, Japan, collaborating with researchers of the Okinawa Centenarian Study. Finally, she is interested in behavioral prevention trials against cognitive decline. She is currently conducting an NIH-funded prevention study to examine whether stimulations through social interaction could improve cognitive function.  She holds Fellow status at the Gerontological Society of America and serves as a statistical editor for several dementia related journals.

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Dr. Dodge’s Mini-Symposium Lecture

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Biomarker Values Predictive of Cognitive Decline in MCI: Baseline or Progression?

Hiroko H. Dodge, Jian Zhu, Danielle Harvey, Naomi Saito, Lisa C. Silbert, Jeffrey A. Kaye, Robert Koeppe, Roger Albin, Oregon Health & Science University, Portland, OR, USA


Background: It is not known which component of commonly employed Alzheimer disease (AD) biomarkers –baseline values or progression of values–is a better predictor of longitudinal cognitive decline.  We examined whether individual differences in cognitive decline are explained better by changes/progression of biomarkers than baseline values at each cognitive stage.


Methods:  526 subjects in the Alzheimer’s Disease Neuroimaging Initiative (ADNI) with valid data in at least one of our variables of interest were used in this study.  The primary clinical outcomes are the ADNI composite memory (ADNI-Mem) and executive (ADNI-Exe) scores. First, individual-specific slope of the longitudinal trajectory of each biomarker was estimated using mixed effects models. These estimates and observed baseline biomarker values were used as predictors of cognitive declines using mixed effects models.  Variability in cognitive decline explained by subject-specific baseline biomarker values was compared with variability explained by biomarker progressions.


Results: Biomarker progressions explained variability in cognitive declines more than baseline values. The highest proportion of variability was explained by ventricular volume progression (39.4% of memory declines, and 44.5% of executive function declines) among MCI, and by FDG-PET score progression (84% of memory decline) and ventricular volume progression (65.1% of executive function declines) among AD.


Conclusions: Biomarker progressions are generally more robust than baseline values in predicting cognitive decline.   This has important implications for clinical trials targeted to modify AD biomarkers, as well as for prognosis and prediction of clinical outcomes.

For the Alzheimer’s Disease Neuroimaging Initiative

Adam S. Fleisher, MD, MAS

Speaker – Workshop

Adam S. Fleisher, headshot_fleisherMD, 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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Dr. Fleisher’s Workshop Lecture

Dr. Fleisher’s Public Educational Forum Lecture

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Biomarker Use to Assist in Diagnosis of Atypical MCI Presentations/ Imaging for identifying non-AD/ Imaging for Identifying Non-AD


Adam S. Fleisher, MD, MAS, Banner Alzheimer’s Institute

Mary Ganguli, MD, MPH

Moderator – Mini-Symposium 2 Discussion

ganguliDr. 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 ( 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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Dr. Ganguli’s Moderated Discussion

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Clifford R. Jack, MD

Speaker – Symposium

headshot_jackDr. Clifford Jack, MD, joined the staff of Mayo Clinic, Rochester in Radiology (Neuroradiology) in 1985. He holds the academic rank of Professor of Radiology and is also recognized with the distinction of a named professorship, the Alexander Family Professor of Alzheimer’s Disease (AD) Research. Dr. Jack has been awarded the Potamkin Prize for Alzheimer’s and Related Diseases from the American Academy of Neurology and also the MetLife Foundation Award for Medical Research in Alzheimer’s Disease. He has also received the Gold Medal from the International Society of Magnetic Resonance in Medicine; the American Society of Neuroradiology Award for Outstanding Contributions in Research; and was elected to the inaugural Council of Distinguished Investigators of the Academy of Radiology Research. His research group develops and validates MR, amyloid and FDG PET analysis methods for diagnosis and measuring progression of Alzheimer’s disease and related disorders. A major effort is directed at modeling interrelationships among cognitive performance, imaging and biofluid biomarkers over time.

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Dr. Jack’s Mini-Symposium Lecture

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The Relationship between Ab Deposition, Neurodegeneration and Cognitive Function in Normal and Impaired Individuals

Clifford R. Jack Mayo Clinic, Rochester MN, USA


Five Alzheimer’s disease (AD) biomarkers are sufficiently validated to have been incorporated into clinical diagnostic criteria and commonly used in therapeutic trials. AD biomarkers fall into 2 mechanistic categories: biomarkers of amyloid-b plaques and of tau-related neurodegeneration. We propose that AD biomarkers do not evolve in an identical manner but rather in a sequential but temporally overlapping manner. Models of the temporal evolution of AD biomarkers can take the form of plots of biomarker severity (degree of abnormality) vs. time.  This presentation will address several time-dependent models of AD which take into consideration varying age of onset, cognitive reserve, and the influence of co-occurring brain pathologies. The common age-associated brain pathologies are AD (plaques and tangles), brainstem and medial temporal lobe tauopathy without amyloid plaques, cerebrovascular disease, alpha synuclein deposits (Lewy bodies), hippocampal sclerosis, and TDP43 inclusions. These same pathologies are found in demented elderly subjects and in elderly subjects who were cognitively normal at the time of death albeit at lower overall pathological burdens than in demented subjects. AD biomarker modeling is discussed from 2 perspectives: early onset which is a reasonable model of “pure AD”; and late onset which usually consists of AD plus one or more co-occurring pathological processes.

Supported by NIH grants R01 AG011378 and R01 AG41851.

William E. Klunk, MD, PhD

Discussant – MiniSymposium 1

  headshot_klunkDr. William E. Klunk is a Distinguished Professor of Psychiatry and Neurology and Co-Director of the Alzheimer Disease Research Center at the University of Pittsburgh and Vice-Chair of the Medical and Scientific Advisory Council of the National Alzheimer’s Association. Dr. Klunk completed an MD/PhD degree at Washington University in St. Louis focusing on neuropharmacology and medicinal chemistry.  Dr. Klunk then completed a general psychiatry residency at the University of Pittsburgh, followed by a Fellowship in Geriatric Neuropsychopharmacology at the same institution.  He has published well over 175 journal articles and book chapters and is Principal Investigator of several NIH and Foundation grants and has received a MERIT Award from the NIA. Dr. Klunk is a pioneer in the field of in vivo amyloid imaging for Alzheimer’s disease.  His work spans from basic synthetic chemistry and neuropharmacological evaluation of amyloid imaging tracers to human PET studies of these tracers.  His group’s 2004 paper was cited by Nature Medicine as the most highly cited research paper on Alzheimer’s disease published since 2004.  He shared the 2004 MetLife Foundation Award, the 2008 Potamkin Prize and the 2009 Ronald and Nancy Reagan Research Institute Awards for research in Alzheimer’s disease with his colleague, Chet Mathis.

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Dr. Klunk’s Moderated Discussion

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Susan M. Landau, PhD

Speaker – Symposium

landauDr. 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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Dr. Landau’s Mini-Symposium Lecture

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Amyloid, Glucose Metabolism, and Longitudinal Change

Susan M. Landau, Helen Wills Neuroscience Institute, University of California, Lawrence Berkeley National Laboratory, Berkeley, California, USA


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.

David Loewenstein, PhD, ABPP

Chair – Mini-Symposium 2

headshot_loewensteinDr. Loewenstein is Director of Neuropsychology and Professor of Psychiatry and Behavioral Sciences at the Miller School of Medicine at the University of Miami. He has been actively involved in collaborative research with Dr. Ranjan Duara and other scientists at the Wien Center for Alzheimer’s Disease and Memory Disorders at Mount Sinai Medical Center, Miami Beach Florida where Dr. Loewenstein served as Director Neuropsychology Laboratories and Research Director for over 20 years. Dr. Loewenstein has a number of research interests centering on the early detection of early cognitive impairment in neurodegenerative and other brain disorders, development of novel cognitive and functional measures, examining relationships between neuropsychological measures, neuroimaging and other biomarkers of early Alzheimer’s disease. Further, Dr. Loewenstein and other investigators in his laboratory have been involved in developing cognitive and functional interventions for normal elderly patients as well as those with Alzheimer’s disease and related disorders.

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Dr. Loewenstein’s Mini-Symposium Lecture

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Development of Novel Paradigms for Assessing and Monitoring Cognitive Change across the MCI and PreMCI Spectrum

David Loewenstein, PhD, ABPP, University of Miami Miller School of Medicine, Miami, FL, USA


 As an emphasis shifts from early detection of dementia to the earliest forms of cognitive impairment, it is imperative to rethink traditional cognitive paradigms that has guided Alzheimer’s disease research. We have found that selective vulnerability to semantic interference is an early marker of early MCI and PreMCI states and is predictive of progression to dementia. These measures also correlate with biomarker status such as amyloid imaging and medial temporal atrophy on MRI.  Category cues at both encoding and retrieval has been long shown by Buschke to provide a measure of maximum storage capacity and can serve to  enhance semantic interference effects and allow the patient to serve as their own controls rather than simply relying on group means  compared to normative data. We discuss the development of newer paradigms that allow the earliest detection of cognitive impairment but have sufficient numbers of layers that make them suitable for tracking change over time. Other paradigms are also considered that may enhance our ability to track very early cognitive impairment and track changes over time.

Chester A. Mathis, PhD

Chair – Mini-Symposium 1

headshot_mathisChester A. Mathis, PhD, is Distinguished Professor of Radiology, Pharmaceutical Sciences, and Pharmacology and Biological Chemistry at the University of Pittsburgh, Director of the University of Pittsburgh Positron Emission Tomography (PET) Facility, and UPMC Endowed Chair of PET Research.  Dr. Mathis has a long-standing interest in applying synthetic radiochemistry techniques to develop PET radiopharmaceuticals to study biological function in vivo.

Over the past 30 years, he has focused primarily on the development of radiotracers to image neuroreceptor systems using PET imaging methodology.  Approximately 18 years ago, he joined efforts with Professor William Klunk of the Department of Psychiatry at the University of Pittsburgh to devise a PET radiotracer capable of imaging amyloid-beta plaques in living human brain. This work led to the successful development of 11C-labeled Pittsburgh Compound-B (PiB) to non-invasively assess amyloid-beta plaque load in the brains of humans using PET imaging.

Elizabeth Mormino, PhD

Speaker – Symposium

headshot_morminoElizabeth Mormino, PhD, is currently a post-doctoral fellow in the laboratory of Reisa Sperling at Massachusetts General Hospital.  She completed her PhD in Neuroscience at UC Berkeley with Dr. William Jagust, where she used multi-modal neuroimaging approaches to examine different aspects of preclinical Alzheimer’s disease—beta-amyloid (Aβ) pathology with PIB PET imaging, neuronal atrophy with structural MRI, and brain activation with functional MRI.       Dr. Mormino is particularly interested in how multiple factors contribute to an individual’s susceptibility to Alzheimer’s disease, and how research using neuroimaging biomarker data in humans will inform secondary prevention trials.  Her recent work has focused on combining data across multiple studies of Alzheimer’s disease development (Harvard Aging Bran Study, ADNI and AIBL), in order to examine how different risk factors may interact to predict longitudinal cognitive decline in clinically normal individuals.

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Dr. Mormino’s Mini-Symposium Lecture

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Cognitive Correlates of Neurodegeneration Related to Beta-Amyloid and Aging in Clinically Normal Individuals

 Elizabeth Mormino, PhD, Massachusetts General Hospital, Boston, MA, USA


Many clinically normal elderly individuals (CNs) have evidence of elevated beta-amyloid (Ab) accumulation, a pathology associated with Alzheimer’s disease (AD).  Evidence of neurodegeneration, such as reductions in gray matter volume and thickness, is also observed in studies of aging.  Research examining associations between elevated Ab and markers of neurodegeneration cross-sectionally have been inconsistent, with some studies showing reduced gray matter in Ab+ CNs (1-3) while others have not (4, 5). However, studies examining associations between Ab status and longitudinal gray matter changes have consistently demonstrated higher rates of atrophy in Ab+ CNs (6, 7).  Furthermore, evidence of neurodegeneration in typical AD regions are observed in Ab- CNs, suggesting that effects of aging are superimposed on brain regions traditionally thought to be vulnerable to AD processes (8, 9). Overall, this pattern is suggestive of 2 pathways that are initially independent—an amyloid pathway that begins late in life and a neurodegeneration pathway that may begin mid-life and progresses slowly until it is accelerated by aberrant Ab accumulation.  Interestingly, correlations between neurodegeneration and cognition are stronger in Ab+ CNs (5), suggesting that the convergence of these 2 pathways may be necessary for AD development.  Large datasets of CNs followed longitudinally will be essential to understand the interaction between Ab accumulation and patterns of neurodegeneration in aging, and the risk factors that promote these pathways.

Denise C. Park, PhD

Speaker – Symposium

Denise C. Pheadshot_parkark, PhD, is Distinguished University Professor of Behavioral and Brain Sciences and University of Texas Regents Research Scholar at the University of Texas at Dallas where she is founder and Codirector of the Center for Vital Longevity.  She is an expert in the cognitive neuroscience of aging, and focuses her research on healthy adults across the entire lifespan.  Dr. Park directs the Dallas Lifespan Brain Study, a NIA-funded longitudinal study that integrates multiple biomarkers, including amyloid imaging, to understand how the brain adapts to neural insults and how cognitive function is affected.  She is a fellow of multiple associations including the American Association for the Advancement of Science, and has held national offices in both the Association for Psychological Sciences and the American Psychological Association.  Dr. Park has published more than 150 articles and six books on the brain and aging. She has been continuously funded by the National Institute on Aging for more than 30 years, including a prestigious MERIT Award.

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Beta Amyloid Deposition in Very Healthy Adults: Risk Factors and Cognitive Consequences

Denise C. Park, PhD, Center for Vital Longevity, University of Texas, Dallas, TX, USA


The Dallas Lifespan Brain Study includes over 300 adults who have been well-characterized cognitively and have completed PET scans with florbetapir f-18 as well as structural and functional MRI.  We report risk factors for beta amyloid deposition related to APOE-4 and uncontrolled hypertension, with evidence that risk is particularly high for adults with uncontrolled hypertension and who are APOE-4 positive.  We also have increasingly strong evidence that young and middle-aged adults who have amyloid deposits higher than their age peers show evidence of lower cognitive performance, suggesting that deposition of amyloid well below clinical cutoffs has an impact at younger ages.

Ronald C. Petersen, MD, PhD

Speaker – Symposium

headshot_petersenRonald 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.

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The Role of Imaging Biomarkers in the Prediction of MCI and Dementia Due to AD

Ronald C. Petersen, MD, PhD, Mayo Clinic, Rochester, MN, USA


As the threshold for making the diagnosis of Alzheimer’s disease (AD) moves earlier in the clinical spectrum, biomarkers become more essential in establishing a diagnosis.  The Mayo Clinic Study of Aging (MCSA) is a population-based study of non-demented individuals ages 50 to 89 years in Olmsted County, Minnesota.  As such, we have collected over 2400 MRI scans and 1200 FDG PET and PiB PET scans in following this cohort.  We have reported data on the role of these imaging biomarkers in predicting the progression from normal aging to mild cognitive impairment (MCI) and from MCI to dementia.  These data will be updated, and the role of the biomarkers in predicting multiple types of dementia will be discussed.

Dorene Rentz, PsyD

Speaker – Forum

headshot_rentzDorene M. Rentz, PsyD, is a clinical neuropsychologist with dual appointments in the Departments of Neurology at Brigham and Women’s Hospital and Massachusetts General Hospital. She is an Associate Professor of Neurology at Harvard Medical School and serves as the Co-Director of the Center for Alzheimer Research and Treatment and the Director of Neuropsychology at the Massachusetts Alzheimer’s Disease Research Center. She is also the Director of Neuropsychology at the Massachusetts Alzheimer Disease Research Center. Dr. Rentz’s research focus has been on the early detection of preclinical Alzheimer’s disease, particularly in high functioning individuals. With Drs. Reisa Sperling and Keith Johnson, her recent work involves exploring early cognitive changes using PET imaging and sensitive memory tests.

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Longitudinal Cognitive and Imaging Changes in a 70 Y/O Woman with Initial Subjective Cognitive Concerns

 Dorene Rentz, PsyD, Harvard Medical School/Brigham and Women’s Hospital, Boston, MA, USA


We will present data of a 70 year old, high school Italian/ English teacher who initially presented with subjective cognitive concerns (SCC) in the context of a family history of Alzheimer’s disease. Initial neuropsychological evaluation was performed in 2007 and repeated in 2011 and 2013. Neuropsychological data, MRI, PIB-PET and Tau T807 PET imaging data will be presented. A discussion of SCC and cognitive reserve will be provided.

Stephen Salloway, MD, MS

Keynote Lecturer – Workshop

headshot_sallowayStephen 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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Challenges in the Diagnosis of Early Alzheimer’s Disease

 Stephen Salloway, The Warren Alpert Medical School of Brown University, Providence, RI, USA


Seventy seven million Baby Boomers will be turning 65 over the next 15 years and the US Congress and the G-8 have made finding treatments to delay or prevent Alzheimer’s disease by 2025 a top priority. The plaques and tangles of AD begin accumulating more than 10 years before the onset of memory loss. Like cancer, heart disease, and HIV, the goal is to begin treatment early to protect the brain before nerve cells begin to degenerate.

Major advances have been made to safely image the buildup of amyloid plaques, a process that previously could only be done through post-mortem examination. This year we will use these amyloid PET scans to launch the first large scale secondary prevention trials for AD. In the anti-amyloid in asymptomatic AD trial, amyloid PET scans will be performed in cognitively normal people, age 65-85, to determine who is at risk for AD. Individuals with positive amyloid scans will receive an anti-amyloid vaccine or placebo for 3 years to try and delay the onset of cognitive decline. The Dominantly Inherited Alzheimer’s Network Trial will test drugs to delay the onset of memory loss in family members with a genetic mutation that causes early onset AD. The Alzheimer’s Prevention Initiative prevention trial will test a new medication in people who carry two copies of an AD risk gene, Apolipoprotein E4 (ApoE4).

These are exciting times in AD research as we rise to meet the global economic and care challenge posed AD for the aging population. This talk will address some of the key factors that need to be overcome to meet the goal of early diagnosis and intervention for AD. 1) Better diagnostic tests and screening methods to differentiate the cognitive decline in early AD from that seen in normal aging. This is especially important for individuals with higher education. 2) The diagnosis of AD may be difficult, even for patients who already have dementia. At least 20% of patients enrolled in recent clinical trials for mild-moderate dementia due to AD do not meet the expected threshold on amyloid PET scans and many of these individuals do not have AD. This proportion is higher for subjects that do not carry and ApoE4 gene. 3) Amyloid and tau biomarkers can detect people at risk for developing AD dementia, but proximity markers are needed to predict the time course of future cognitive decline. 4) Amyloid PET scans are specific for detecting fibrillar amyloid pathology, but scans need to be interpreted with care, especially in intermediate cases, as amyloid buildup can be present in a variety of conditions, including normal aging. 5) AD presents with an amnestic phenotype in the majority of cases. However, in a recent large series at least 11% of subjects had hippocampal-sparing AD post-mortem. 6) We need to be better able to assess the important contribution of co-morbid conditions such as cerebrovascular disease and chronic medical illnesses in patients with late-onset cognitive disorders. 7) Our current biomarkers can be used for secondary prevention trials but primary prevention will require the identification of genetic and biochemical markers present before the accumulation of amyloid and tau. 8) Because of the size of the risk population, we need to ensure wide access to biomarkers and broader training for non-dementia specialists, especially in primary care.

Philip Scheltens, MD, PhD

Speaker – Workshop


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 (Vrije Universiteit) Medical Center, 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, as well as Honorary Professor of Neurology at University College London. 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 (inter) national PI for many studies, including Phase I–III multicentre clinical trials. He is founder of, and has directed since 2000, the Alzheimer Center, which during this time has produced over 34 PhD theses. Dr. Scheltens is an active member of several societies, including the Dutch Society for Neurology, the IPA, the AAN, the Alzheimer Imaging Consortium, the ISTAART Consortium, and the ECNP. He has been instrumental in organising several national and international conferences, including the Imaging Symposium attached to ICAD. He chairs the dementia panel of the EFNS. He was Associate Editor of the Journal of Neurology, Neurosurgery and Psychiatry until 2010. He was Chief Editor of the official journal of the Dutch Society of Neurology until November 2008. He is also a member of the editorial boards of Dementia and Geriatric Cognitive Disorders and International Journal of Geriatric Psychiatry, and acts as an ad hoc reviewer of scientific articles for, amongst others, The Lancet (Neurology), Stroke, Neurology, Annals of Neurology, New England Journal of Medicine, Brain, and Science a.o. He has authored >510 peer reviewed papers and >50 book chapters. Dr. Scheltens co-edited the books, Magnetic Resonance in Dementia (Springer), Neuroimaging in dementia (Springer) and Functional Magnetic Resonance Imaging: Clinical Applications (Oxford University Press). He was one of the founding fathers of, and has acted as Treasurer of the International Society for Vascular Behavioural and Cognitive Disorders (Vas-Cog), until 2011. He was elected member of the Royal Academy of Arts and Sciences in 2011 and act as secretary of the Medicine Section since 2012.

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Conflicting Biomarkers in Clinical Practice

Philip Scheltens, MD, PhD, VU University Medical Center, Amsterdam, Netherlands


Biomarkers for Alzheimer’s disease are CSF abeta, tau and p-tau and well as amyloid PET. I will describe 2 cases in which discrepancies were found between these two sorts of biomarkers in patients clinical diagnosed with AD. Consequences for clinical practice including management of the patient will be discussed.

Ben Schmand, PhD

Speaker – Symposium


Dr. Ben Schmand is professor of clinical neuropsychology at the University of Amsterdam, and is affiliated with the neurology department of the Academic Medical Center in Amsterdam. His research involves applied neuropsychological topics such as development of new cognitive tests, efficiency of neuropsychological assessment, cognitive impairment in neurological and psychiatric diseases, and neuropsychological (side) effects of medical treatments.

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On Cognitive Performance as the Endpoint in Clinical Trials

Ben Schmand, PhD, University of Amsterdam, Amsterdam, Netherlands


Measurement of cognitive impairments has always been important in intervention studies AD. This is inevitable, because the disease is defined by cognitive symptoms. Typical cognitive outcome measures in pharmacological research on AD are so-called omnibus tests, such as the cognitive section of the Alzheimer’s Disease Assessment Scale. These tests are inherently weak from a psychometric point of view, and they are unsuitable as endpoints in clinical trials with MCI patients. As a result, there is a tendency to replace cognitive measures by neuroimaging and neurochemical biomarkers as endpoints in intervention research on MCI.

This contribution will discuss why cognitive performance remains the most relevant endpoint, which types of cognitive tests serve this purpose best, and how test results should be handled in order to obtain a most responsive endpoint. These issues will be illustrated with empirical data, comparing cognitive endpoints with neuroimaging and neurochemical outcome measures.

Frederick A. Schmitt, PhD

Speaker – Symposium

headshot_schmittFrederick A. Schmitt, Ph.D. is a Professor of Neurology with joint appointments in the Departments of Psychiatry, Psychology, Neurosurgery, and Behavioral Science.  He also holds an appointment as a Center Associate in the Sanders-Brown Center on Aging and Spinal Cord and Brain Injury programs at the University of Kentucky (UK).  He is a clinical scientist with a primary focus on the evaluation of the relationship between physiological changes associated with normal aging, Down syndrome, and dementia associated with neurodegenerative diseases.

Dr. Schmitt has been an investigator on multiple multidisciplinary program project grants, the Alzheimer’s Disease Center at UK where he works in the Clinical and Biostatistics Cores.  He has coordinated multiple studies of experimental therapies for MCI and AD.  His present research, along with his colleagues, involves an antioxidant AD prevention trial (with over 7,500 participants), statistical models of mixed dementia neuropathology, as well as diffusion tensor imaging and plasma proteomics as predictors of dementia evolution in Down syndrome.

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Probability of Transition To and From MCI: Models of Clinical and Cognitive Features

Frederick A. Schmitt, University of KentuckySanders-Brown Center on Aging, Lexington, KY, USA


Predicting the change from normal cognitive aging to mild cognitive impairment (MCI) and dementia, as well as time spent with an MCI diagnosis, has been a focus of population-based and longitudinal cohort studies.  Predictors have included demographic, genetic, cognitive, and imaging with some analyses incorporating neuropathological findings.  With the publication of new research criteria for MCI1, the determination of MCI risk factors deserves renewed scrutiny.

While MCI appears to have clear neuropathological underpinnings2,3, the clinical diagnosis of MCI has often been reported as ‘unstable’ with low conversion rates in population-based analyses.4  New applications of probability models for normal cognitive aging, MCI, and dementia provide an alternative approach to understanding risks.  Risk factors for MCI transitions, time to conversion (transition), as well as new concepts of ‘test-based’ and ‘consensus-based’ MCI classifications along with subjective memory complaint will be presented as potential markers of MCI development and evolution to dementia.  Analyses provide approaches that harmonize the literature on MCI diagnosis and can serve to inform prevention and treatment trials in MCI as well as preclinical dementia.


1.   Budson AE, Solomon PR. New diagnostic criteria for Alzheimer’s disease and mild cognitive impairment for the practical neurologist. Pract Neurol. 2012 Apr;12(2):88-96.

2.   Markesbery, W.R., Schmitt, F.A., et al. (2006).  Neuropathological substrate of mild cognitive impairment. Archives of Neurology, 63, 38-46.

3.   Schmitt, F.A., Davis, D.G., Wekstein, D.R., Smith, C.D., Ashford, J.W., & Markesbery, W.R. (2000). “Preclinical” AD revisited: neuropathology of cognitively normal older adults. Neurology, 55, 370-376.

4.   Ritchie K, Artero S, Touchon J. Classification criteria for mild cognitive impairment: a population-based validation study. Neurology. 2001 Jan 9;56(1):37-42.

Beth Snitz, PhD

Speaker – Symposium

headshot_snitzBeth Snitz, PhD, is an assistant professor of Neurology at the University of Pittsburgh School of Medicine. She received her doctoral degree in clinical psychology from the University of Minnesota. She is a co-investigator with the University of Pittsburgh Alzheimer’s Disease Research Center, Clinical Core Leader for the ADRC-affiliated PiB-PET Program Project Grant, and co-investigator on the Monongahela-Youghiogheny Healthy Aging Team (MYHAT) Study, a population study of MCI in southwest Pennsylvania.

Dr. Snitz’s current research focuses on boundaries between normal and pathologic cognitive aging, including mild cognitive impairment, cognitive correlates of amyloid imaging in normal aging, and subjective cognitive complaints in clinic and community.

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Cognitive Trajectories Associated with β-amyloid Deposition in Normal Aging and MCI

Beth Snitz, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA


The goal of this study was to determine whether a high prevalence (55%) of Aβ deposition in a cohort of individuals remaining dementia-free into their 9th and 10th decades was associated with cognitive decline prior to amyloid imaging. A total of 194 participants (mean age 85.5 years) who completed the Ginkgo Evaluation of Memory Study (GEMS) and remained dementia-free subsequently completed PiB–PET imaging. We examined cross-sectional associations between Aβ status and performance on a broad neuropsychological test battery completed at GEMS entry 7–9 years prior to neuroimaging. We also longitudinally examined cognition over annual evaluations using linear mixed models. Highly prevalent Aβ deposition in oldest-old adults was associated with cognitive decline in visual memory, semantic fluency, and psychomotor speed beginning 7–9 years prior to neuroimaging. Mean differences in non-memory domains, primarily executive functions, between Ab-status groups were detectable 7–9 years before neuroimaging. Objective and subjective cognitive correlates of Aβ in younger-old normal aging studies will also be compared and discussed.

David A. Wolk, MD

Speaker – Symposium, Workshop and Forum

headshot_wolkDr. David Wolk is an Associate Professor of Neurology in the Cognitive Neurology Division of the University of Pennsylvania Perelman School of Medicine. He is also Assistant Director of the Penn Memory Center. His primary clinical interest has been in the diagnosis and care of individuals with a variety of neurodegenerative conditions.

Dr. Wolk’s research has focused on the cognitive neuroscience of memory decline associated with aging and Mild Cognitive Impairment/Alzheimer’s Disease using techniques including behavioral testing, Event-Related Potentials, structural and functional MRI, and amyloid PET imaging. A highly related additional line of his work has been the development and examination of biomarkers for detection of early disease changes that differentiate normal aging from evidence of neurodegenerative pathophysiology. This work has also included use of morphometric structural imaging methods, MRI measures of cerebral blood flow, and molecular imaging techniques. In addition to early disease detection, Dr. Wolk has explored the relationship of these measures to phenotypic variation for trying to better understand heterogeneity in these populations.

Dr. Wolk completed his medical training at Johns Hopkins University, a Neurology residency at the University of Pennsylvania, and clinical Fellowship training in Cognitive and Behavioral Neurology at Brigham and Women’s Hospital/Harvard Medical School; where he also completed a post-doctoral research fellowship studying memory in Alzheimer’s Disease. Amongst a number of honors, he is the recipient of the American Academy of Neurology’s Norman Geschwind Prize in Behavioral Neurology.

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Clinical Implications of Concordant and Discordant Beta-Amyloid and Neurodegenerative Abnormalities in Mild Cognitive Impairment

David A. Wolk, MD, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA


Recent criteria for Mild Cognitive Impairment (MCI) incorporates the use of biomarkers that detect either the presence of cerebral amyloidosis (CSF Aβ, amyloid PET imaging) or evidence of neurodegeneration (structural MRI, FDG PET, CSF tau).  Based on the results of these biomarkers (‘positive’, ‘negative’, ‘indeterminate’) an algorithm has been developed for assessing the likelihood that MCI is due to AD based on the existing literature.  Since these criteria were proposed in 2011, much additional data, as well as analyses of prior data based on this framework, have accrued in MCI patients in whom multiple biomarker have been obtained to allow for some verification of this scheme.

In this talk, I will present data on the clinical implications of both concordant and discordant results of biomarker studies in MCI, particularly markers of β-amyloid versus neurodegeneration.  In addition to having implications for the likelihood of developing clinical AD, I will review data that suggest that the relationship of these biomarkers also has important predictive value regarding the timing of clinical conversion.  More specifically, neurodegenerative markers appear to provide finer temporal information consistent with models of the pathophysiologic and biomarker cascade of AD.  However, there are reported instances in which the combination of biomarker findings are not clearly in keeping with this model (e.g. the presence of evidence of neurodegeneration in those with a ‘negative’ beta-amyloid study) ,and we will discuss the clinical implications and potential interpretations of these cases.  Nonetheless, despite some degree of uncertainty in select situations, the majority of data in MCI support the complementary value of biomarkers of cerebral amyloidosis and neurodegeneration.