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13th International Conference on Myasthenia Gravis


for Members

13th International Conference on Myasthenia Gravis

Tuesday, January 24, 2012

The New York Academy of Sciences

Alzheimer's disease (AD) is set to become the most devastating health care crisis facing society in the 21st century as we shift toward an increasingly elderly demographic. With the advent of new clinical tools, there is an increasing appreciation that the events leading to AD may begin years and even decades prior to diagnosis. The availability of amyloid imaging agents provides one striking example: Fibrillar amyloid deposits, once considered "tombstone markers" occurring well after diagnosis of AD, are now known to occur a decade or more prior to diagnosis on average. The goal of this symposium is to explore an integrated view of the structural, functional, and biochemical events that may precede and predict both AD and amnestic mild cognitive impairment (aMCI). The available tools include imaging agents for amyloid deposits, FDG-PET, structural MRI, default network functional MRI, and a plethora of potential CSF and plasma biochemical markers. Developing and refining this integrated view of what these clinical tools are able to reveal is essential to gaining clues about key causal events leading to AD, to understanding how measurable functional deficits in the brain might be detected behaviorally, and to establishing and validating surrogate biomarkers predictive of AD onset.

Reception to follow.

Registration Pricing

Student / Postdoc / Fellow Member:$0
Student / Postdoc / Fellow Nonmember:$15


Presented by

  • American Chemical Society, New York Section
  • The New York Academy of Sciences

Gold Sponsor

  • Pfizer


* Presentation times are subject to change.

Tuesday, January 24, 2012

12:30 PM


1:00 PM

Robert B. Nelson, PhD, Lundbeck Research USA

1:10 PM

Molecular and Functional Imaging of Preclinical Alzheimer's Disease: Defining Cohorts for Secondary Prevention Trials
Reisa Sperling, MD, Brigham and Women's Hospital and Harvard Medical School

1:50 PM

New Perspectives on 'Silent' Brain Amyloidosis: Relationships to Other Markers of Preclinical AD and Risk for AD Dementia
John C. Morris, MD, Washington University School of Medicine

2:30 PM

White Matter Microstructural Alterations: Relation to other Markers of Preclinical Alzheimer's Disease
Brian T. Gold, PhD, University of Kentucky

3:10 PM

Coffee Break

3:40 PM

Cognitive ERPs as Biomarkers for Very Early Alzheimer's Disease
John Olichney, MD, University of California, Davis

4:20 PM

Plasma and CSF-based Biomarkers for MCI and AD: Relationship to Pathogenesis, Conversion, and Progression Rate
Simon Lovestone, PhD, MRCPsych, MRC Centre for Neurodegeneration Research, London

5:00 PM

Networking Reception

6:00 PM

Program Ends



Robert B. Nelson, PhD

Lundbeck Research USA

Bob Nelson is a Research Fellow at Lundbeck Research USA, a company specializing in the development of therapeutics for CNS diseases. Previous to joining Lundbeck in 2010, Bob was a research investigator at Pfizer and overall has 20 years of experience in the pharmaceutical industry. Bob received his doctorate from Northwestern University in 1987 followed by two post-doctoral fellowships working in the laboratories of Robert Siman at DuPont and Huntington Potter at Harvard Med School. Bob now leads one of two research groups at the Lundbeck site in Paramus, NJ, investigating how changes in the immune system initiate or promote Alzheimer's and other neurological diseases, with the goal of designing therapeutics that arrest these pathological changes. The Lundbeck Neuroinflammation unit takes a broad view of seeking the best disease intervention points by studying the interactions between the two main arms of the immune system (innate and adaptive), and the interactions between vascular immune cells (such as monocytes and T-cells) and the brain's immune cells (such as microglia and astrocytes).

Robert L. Martone

Covance Biomarker Center of Excellence

Robert Martone is Neuroscience Therapeutic Area Lead for the Covance Biomarker Center of Excellence. He has extensive experience in the pharmaceutical industry leading neuroscience drug discovery and technology teams through all phases of discovery from target identification through clinical trials with expertise in both small molecule and protein therapeutics. He also has several years of academic research experience in molecular neurobiology, with a focus on the molecular genetics of familial neuropathies, and CNS tumor biomarker development.

Ken Jones, PhD

Forest Research Institute

Ken received his PhD in Physiology at Rutgers University studying neuronalnetworks that control behaviors of model organisms. During postdoctoral training at Harvard Medical School with Robert Baughman he developed mammalian primary cell culture techniques to map NMDA and AMPA receptors at synaptic and extrasynaptic sites. His subsequent research in biotech and pharmaceutical companies has provided a number of promising novel drug targets for psychiatric and neurological disorders. At Synaptic Pharmaceutical Corp he co-discovered the heterodimeric nature of GABAB receptors, a newphotoreceptor that regulates circadian rhythms, as well as several novel hypothalamic neuropeptide receptors. In his most recent position at Lundbeck Research (Paramus, NJ) he was responsible for capital and process improvements that dramatically improved assay throughput in the HTS group, and he served leadership roles in a handful of early to late-stage drug discovery projects. He has enjoyed co-organizing a variety of NYAS symposium under the auspices of the Biochemical Pharmacology Discussion Group.

Jennifer Henry, PhD

The New York Academy of Sciences


Brian T. Gold, PhD

University of Kentucky

Dr. Gold is an Associate Professor in the Department of Anatomy and Neurobiology at the University of Kentucky (UK) College of Medicine. He is also a faculty affiliate of UK's Sanders-Brown Center on Aging and Magnetic Resonance Imaging Center. Dr. Gold is the Director of the Cognitive Neuroscience Laboratory at UK, serving as a mentor to postdoctoral scholars, graduate students, and undergraduate researchers. Dr. Gold received his Ph.D. in psychology (cognitive neuroscience focus) from York University in 1999. He then did his postdoctoral training at Washington University. Dr. Gold's research focuses on characterizing cognitive and brain changes associated with normal aging, early Alzheimer's disease (AD), and preclinical AD. In addition, he is investigating how certain lifestyle variables (e.g., exercise, education) may slow cognitive decline and brain aging. A multimodal imaging approach is employed, making use of functional magnetic resonance imaging and structural imaging methods such as volumetric assessment and diffusion tensor imaging. Dr. Gold's research is funded through grants from the National Institutes of Health and National Science Foundation. Dr. Gold is currently on the editorial board for the Journal of Alzheimer's Disease and serves as an ad hoc reviewer for many top neuroscience journals. Dr. Gold serves on several scientific advisory boards including the Scientific Advisory Committee for Dementia Research and Prevention, Pennington Biomedical Research Center.

Simon Lovestone, PhD, MRCPsych

MRC Centre for Neurodegeneration Research, London

Simon Lovestone is Director of Research, King's Health partners (, Professor of Old Age Psychiatry at the Institute of Psychiatry, King's College London ( and director of the NIHR Biomedical Research Centre for Mental Health and Unit for Dementia at the South London and Maudsley NHS Foundation Trust and King's College London ( He has research interests in the regulation of tau phosphorylation and in the search for genetic and other biomarkers of Alzheimer's disease and related conditions.

John C. Morris, MD

Washington University School of Medicine

John C. Morris, MD, is the Harvey A. and Dorismae Hacker Friedman Distinguished Professor of Neurology; Professor of Pathology and Immunology; Professor of Physical Therapy; Professor of Occupational Therapy; and Director of the Charles F. and Joanne Knight Alzheimer's Disease Research Center, Memory and Aging Project at Washington University School of Medicine. He is also Director of the Harvey A. and Dorismae Friedman Center for Aging at Washington University. Dr. Morris earned his medical degree from the University of Rochester School of Medicine and Dentistry in Rochester, New York. He completed residencies in internal medicine at Akron General Medical Center and in neurology at the Cleveland Metropolitan General Hospital, both in Ohio, and a postdoctoral fellowship in neuropharmacology at Washington University School of Medicine. Research interests of Dr. Morris include healthy aging and Alzheimer dementia, antecedent biomarkers for Alzheimer's disease in nondemented elderly to evaluate risk for Alzheimer dementia, and trials of investigational drugs for the treatment of Alzheimer dementia.

Dr. Morris has authored or coauthored 4 books and more than 350 published articles. Dr. Morris is a member of several professional societies, including the American Academy of Neurology and the American Neurological Association, and serves on the editorial board for the Annals of Neurology. He serves also on numerous scientific and community advisory boards, including the Medical and Scientific Advisory Council of the national Alzheimer’s Association. He has received many honors and awards, including the Lifetime Achievement Award from the Alzheimer’s Association (2004); the MetLife Award for Medical Research in Alzheimer’s Disease (2004); the Potamkin Prize for Research in Pick’s, Alzheimer’s, and Related Dementias from the American Academy of Neurology (2005); the Physician-Scientist Lifetime Achievement Award, Barnes-Jewish Hospital Foundation, St. Louis, MO (2005); Neville Grant Award for Clinical Excellence from Barnes-Jewish Hospital, St. Louis, MO (2006); Washington University Academic Women’s Network Mentor Award (2008); the American Neurological Association 2009 Soriano Lectureship; and the Carl and Gerty Cori Faculty Achievement Award, Washington University (2010). He is ranked in the top 1% of investigators in the field of Neuroscience and Behavior by Essential Science Indicators database.

John Olichney, MD

University of California, Davis

Dr. Olichney grew up in New York and graduated from Stuyvesant High School. He did his undergraduate work at UC Berkeley and received a Bachelor's degree in Neurobiology. Dr. Olichney attended medical school at University of California, Irvine. He completed his neurology residency at UC San Diego, where he also completed three years of fellowship training—two years in Geriatric Neurology and one year in Traumatic Brain Injury and Neuroscience. His mentors at UCSD included fellowship director Dr. Leon Thal, Dr. Vicente Iragui, Robert Katzman and Professors Marta Kutas and David Salmon. In 1995, Dr. Olichney joined the Department of Neurosciences faculty at University of California, San Diego, where he served as Assistant and Associate Professor. In 2006, he transferred to UC Davis, where he is currently Professor of Neurology, and serves as Clinical Core Leader for their NIA-funded Alzheimer's Disease Center. He is responsible for overseeing a large multi-disciplinary clinical research program in dementia, including their Alzheimer's disease clinical trials unit. He also directs the Cognitive Electrophysiology and Neuroimaging (CEaN) Laboratory in the Center for Mind and Brain in Davis, where he is active in translational cognitive neuroscience research. His main research focus is on the physiology of human memory function during normal aging and disease, using the techniques of event-related potentials (ERPs) and functional MRI (fMRI). His research has been funded by multiple NIH/NIA grants, private foundations (including two NARSAD awards), the Dept. of Veteran's Affairs, and the state of California's Alzheimer's Disease Program. He is also currently participating in four multi-center clinical trials as UC Davis' site principal investigator. He has authored or co-authored over 45 scientific articles published in the medical literature.

Reisa Sperling, MD

Brigham and Women's Hospital and Harvard Medical School

Dr. Reisa Sperling is a neurologist, specializing in dementia and imaging research, and an Associate Professor in Neurology at Harvard Medical School. Dr. Sperling is the Director of the Center for Alzheimer Research and Treatment at Brigham and Women's Hospital and serves as the Director of the Alzheimer's disease Neuroimaging Program of the Massachusetts Alzheimer's Disease Research Center at Massachusetts General Hospital. Dr. Sperling's research is focused on the early diagnosis and treatment of Alzheimer's disease. She is the Principal Investigator on multiple NIH and Foundation grants including a new National Institute on Aging Program Project grant—the Harvard Aging Brain Study—and oversees a number of clinical trials of potential disease-modifying therapeutics in early Alzheimer's disease. She was recently chosen to lead the National Institute on Aging–Alzheimer's Association working group to develop recommendations for the study of "Preclinical Alzheimer's disease."

* Additional bios to follow.


For sponsorship opportunities please contact Carmen McCaffery at or 212.298.8642.

Gold Sponsor

  • Pfizer

Promotional Partners

Alzheimer Research Forum

Biomarker Commons

The Dana Foundation

Academy Friends


Lundbeck Research USA

Mission Partner

The Biochemical Pharmacology Discussion Group is proudly supported by:

  • Pfizer

Grant Support

Elan Pharmaceuticals


White Matter Microstructural Alterations: Relation to other Markers of Preclinical Alzheimer's Disease
Brian T. Gold, PhD, University of Kentucky College of Medicine

Modern neuroimaging techniques promise to sharpen the early diagnosis of Alzheimer's disease (AD). Objective neuroimaging biomarkers may be particularly useful if they can identify preclinical AD states, when emerging interventions are most likely to be successful. The advent of magnetic resonance diffusion tensor imaging (MR-DTI) has made it possible to explore AD-based WM microstructural alterations in vivo. A growing body of research suggests that alterations in WM microstructure are evident prior to significant cognitive decline associated with AD. For example, there is evidence that WM microstructural alterations can be detected in the typical AD-prodromal state of amnestic mild cognitive impairment (aMCI) and even in cognitively normal individuals at risk for future AD. Results from multi-modal imaging studies suggest that WM microstructural declines are not a secondary consequence of macrostructural atrophy in preclinical AD. In addition, the use of WM integrity information appears to improve the classificatory accuracy of aMCI participants compared to the use of gray matter atrophy markers alone. Taken together, these results suggest that WM microstructural alterations appear to provide unique information distinct from macrostructural atrophy measures and may thus aid the imaging contribution to early AD diagnosis. Longitudinal studies are required to determine if WM integrity markers can predict conversion to aMCI or AD.

Plasma and CSF-based Biomarkers for MCI and AD: Relationship to Pathogenesis, Conversion, and Progression Rate
Simon Lovestone, PhD, MRCPsych, MRC Centre for Neurodegeneration Research, London

Considerable progress continues to be made in the search for molecular markers relevant to dementia. Markers for preclinical or prodromal states and predictive of progression to dementia are perhaps the most urgently sought for both clinical practice and for clinical trials. Markers for diagnosis and for prognosis would also have considerable value and both might be used in stratified trials. CSF markers include Abeta and tau, both total and phosphorylated, and these markers have been shown to have value in diagnosis and to contribute to prediction of progression from MCI to dementia. Alone however, the predictive value is probably insufficient and CSF as a marker fluid has limitations especially in the frail elderly and where multiple measures may be needed. Although not in direct contact with brain, increasing evidence suggests a protein signal in plasma that might have utility as a biomarker but there is no consensus yet as to what exactly constitutes the signal. Nonetheless it is clear that inflammatory and acute phase proteins including clusterin, cytokines, A2M and some complement proteins are altered in plasma in AD with some evidence that a marker combination might be predictive of conversion to dementia.

Silent Brain Amyloidosis: Relationships to other Markers of Preclinical AD and Risk for AD Dementia
John C. Morris, MD, Washington University School of Medicine

New diagnostic criteria for symptomatic Alzheimer's disease (AD)now suggest the inclusion of AD biomarkers to enhance the diagnostic process. Such biomarkers can be categorized as secondary, indicating that they are downstream of the primary pathological processes of AD, or molecular, indicating that they detect abnormalities in proteins that are believed to be intrinsic factors in the causation of AD. Secondary biomarkers include volumetric loss (either whole brain or regional, such as in the hippocampus) as shown by structural neuroimaging and metabolic perturbations of glucose or oxygen, as shown by tracer studies with positron emission tomography (PET). Molecular biomarkers include cerebrospinal fluid (CSF) levels of amyloid-beta (Aβ) and tau (either total tau or phosphorylated tau) and PET imaging with amyloid tracers such as Pittsburgh Compound B (PIB).To date, AD biomarkers have been used primarily in research studies. Many more studies are needed to determine their sensitivity and specificity in nonresearch samples for discriminating symptomatic AD from cognitively healthy aging and from other dementing disorders. Moreover, molecular biomarkers identify AD pathology in a subset of cognitively normal older adults2 but too few longitudinal data currently are available to know the true predictive power of the biomarkers for future development of symptomatic AD. Nonetheless, biomarkers are beginning to be used in the clinical setting.The transition to clinical use may be accelerated with the advent of imaging Aβ tracers that will be much more accessible to practitioners than current tracers such as PIB. Familiarity with AD biomarkers will be essential for clinicians to improve diagnostic accuracy for symptomatic AD. They also eventually may be used to select individuals with appropriate molecular targets for "disease modifying" agents, both in treatment trials of symptomatic AD as well as preventive trials for preclinical (presymptomatic) AD.

Cognitive Event-related Potentials as Biomarkers for Very Early AD
John Olichney, MD, UC Davis

There is a recent resurgence of interest in ERP & EEG methods sensitive to the synaptic dysfunction of early stage AD. This talk will review clinical data from cognitive ERP paradigms sensitive to subtle cognitive changes, which occur early in the AD disease process. In particular, ERP studies of memory and language processes, and late components (e.g. P600, N400) which have demonstrated sensitivity to AD, will be emphasized. The evidence that ERPs can be useful to predict prognosis in MCI and the earlier "preclinical" stages of disease will be discussed. The talk will also shed light on how ERPs may play a valuable role in AD clinical trials and drug development, with utilities in cohort selection, monitoring disease progression and cognitive improvement.

Molecular and Functional Imaging of Preclinical Alzheimer's Disease: Defining Cohorts for Secondary Prevention Trials
Reisa Sperling, MD, Brigham and Women's Hospital and Harvard Medical School

The pathophysiological process of Alzheimer's disease (AD) is thought to begin years, if not decades, prior to the onset of clinical dementia. Converging data from PET amyloid imaging and cerebrospinal fluid studies suggest that approximately one-third of clinically normal older individuals harbor a substantial burden of cerebral amyloid-β. Recent multi-modality imaging studies, using PET amyloid imaging and functional MRI, have demonstrated that amyloid deposition in key nodes of the default network is associated with aberrant default network fMRI activity during the encoding of new memories, as well as disrupted default network connectivity at rest. A small number of studies have also reported an association between higher amyloid burden and lower memory performance even among the range of clinically normal older individuals. These findings provide support for the hypothesis that amyloid pathology is linked to synaptic dysfunction in the networks supporting memory processes, detectable prior to the emergence of significant cognitive impairment. Longitudinal studies are ongoing to determine if these amyloid positive older individuals are in the preclinical stages of AD, and are at increased risk for cognitive decline and development of AD dementia. A number of secondary prevention trials are being planned in both genetic at-risk and amyloid-positive older populations, including the "A4" trial: Anti-Amyloid Treatment in Asymptomatic AD.

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