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Successful Targeting of Alzheimer’s Disease - Header

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7:45 am Registration and Morning Coffee

8:20 Chairperson’s Opening Remarks

William J. (Jim) Ray, Ph.D., Senior Director, Neurobiology, Envoy Therapeutics

8:25 OPENING KEYNOTE: Impact of Pre-Competitive Collaboration on Alzheimer’s Disease Drug Development in Europe

Olivier Blin, M.D., Ph.D., M.B.A., Head CIC-CPCET, Clinical Pharmacology, Timone University Hospital, Marseille, France

8:55 Anti-Abeta Immunotherapy for the Treatment of Alzheimer’s Disease

Gene Kinney, Ph.D., Vice President, Head of Research, Janssen Alzheimer Immunotherapy

9:25 New Criteria for AD

Bruno Dubois, Ph.D., Director, Institut de la Mémoire et de la Maladie d’Alzheimer (IMMA), Director, INSERM Group (ICM), Hôpital La Salpêtrière, France

9:55 Networking Coffee Break

Human Genetics

10:25 What can Recent Genetic Findings Teach us About Novel Therapeutics for Alzheimer’s Disease?

Rudolph E. Tanzi, Ph.D., Joseph P. and Rose F. Kennedy, Professor of Neurology, Harvard Medical School; Director, Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease

Alzheimer’s disease (AD) is strongly influenced by inheritance and genetic susceptibility. The four known AD genes, APP, PSEN1, PSEN2, and APOE, account for less than 50% of the genetic variance of AD. We and others have carried out genome-wide association studies to identify novel AD genes. The top results and gene candidates emerging from these studies will be summarized focusing on implications for therapeutic strategies aimed at treating and preventing AD.

10:55 A TOMM-40 Variable Length Polyt Repeat Polymorphism, Inherited through Evolution, Determines the Age of Onset Distribution of Late-Onset Alzheimer’s Disease

Allen D. Roses, M.D., Director, Deane Drug Discovery Institute, Duke University

We sequenced the linkage disequilibrium region containing TOMM-40 and APOE in multiple AD patients and controls, and analyzed the region with phylogenetic mapping technologies. We found a variable polyT polymorphism [rs10524523, aka “523”] inherited on each allele, with multiple polymorphisms inherited over evolutionary time.

11:25 Genome-Wide Association Analyses of Alzheimer’s Disease in Cohorts: Will it Change AD Prevention and Treatment?

Sudha Seshadri, M.D., Associate Professor of Neurology, Co-Director of Medical Education for the Residency Program, Boston University School of Medicine, Senior Investigator, The Framingham Study 

Genome wide association analyses have, in the past two years, identified novel genes besides APOE that alter the risk of late-onset AD. These include CLU, PICALM, CR1 and BIN1. These genes strengthen evidence for involvement of inflammation, lipids and clathrin-mediated endocytosis but also point to novel pathways that merit further study. It is likely the expanded understanding of biology will lead to new drugs and pharmacogenomic targeting of prevention and treatment in AD over the next decade.    

11:55 Luncheon Presentations (Sponsorship Opportunities Available) or Lunch on Your Own


Imaging & Biomarkers

1:30 pm Chairperson’s Remarks

Corinne E. Augelli-Szafran, Ph.D., Director, Experimental Alzheimer Drugs (LEAD), Center for Neurologic Diseases, Brigham and Women’s Hospital; Department of Neurology Harvard Medical School

1:35 The Impact of the ADNI on Drug Discovery & Development

William Z. Potter, M.D., Ph.D., Foundation for NIH Biomarkers Consortium

The FDA, academia and industry are near alignment around a path for developing treatments for pre-symptomatic AD, an alignment that has been made possible through the implementation of the Alzheimer’s Disease Neuroimaging Initiative (ADNI). ADNI was based on solid findings from the field that there were alterations in brain structure and function in individuals diagnoses with AD.

2:05  Early Detection of Alzheimer’s Disease: Are CSF Biomarkers Ready for the Challenge?    

Leslie Shaw, Ph.D., Director, Toxicology Laboratory, Biomarker Research Laboratory, Pathology & Laboratory Medicine, University of Pennsylvania Medical Center

2:35 Neuroimaging Predictors of Cognitive Change: Findings from the Baltimore Longitudinal Study of Aging    

Susan M. Resnick, Ph.D., Senior Investigator, Cognition Section, Laboratory of Personality and Cognition, NIA/NIH

Sponsored by
3:05 Novel Tissue and CSF Biomarkers Targeting Causal Pathways and Network Dynamics in Neurodegenerative Disease
Mahalakshmi “Shubha” Shankaran, Ph.D., Director, Neurobiology, Kinemed, Inc.
Biomarkers of causal pathways in neurodegenerative diseases are needed for developing successful therapeutics. Using stable isotope labeling and mass spectrometry, we have developed tissue biomarkers for key neuronal pathways. Our translational CSF biomarkers measure neuronal transport of specific cargo proteins and dynamic changes in the proteome of neurodegenerative disease patients.

3:35 Grand Opening Refreshment Break in the Exhibit Hall

4:35 ASL Perfusion MRI as a Biomarker of Disease Progression and Therapeutic Response in AD

John A. Detre, M.D., Professor, Neurology and Radiology, Director, Center for Functional Neuroimaging, University of Pennsylvania

Arterial spin labeled (ASL) perfusion MRI allows cerebral blood flow (CBF) to be quantified noninvasively and relatively inexpensively using instrumentation that is widely available. A growing body of evidence suggests that cerebral blood changes correlate with neural dysfunction in Alzheimer’s disease, and can be used to predict and monitor disease progression. Changes in regional CBF also appear to reflect pharmacological actions, providing a biomarker of drug target, dose effects, and possibly a predictor of treatment response. Because ASL perfusion MRI quantifies a biological parameter, it is theoretically independent of scanner platform, and hence well suited for multisite studies.

5:05 A Novel Blood Based Biomarker Assay for Alzheimer’s Disease

Muralidhar Reddy Moola, Ph.D., Associate Professor, Department of Chemistry, The Scripps Research Institute 

A novel unbiased approach to identifying disease-related antibodies, using combinatorial organic chemistry, involves the production of peptoid microarrays. We believe that the peptoids mimic some aspect of the shape of the (unknown) native antigen(s) recognized by the AD-specific antibodies, and thus serve as relatively high affinity capture agents. Validation of these peptoid biomarkers using a larger sample of AD patients can lead to a useful biomarker for the disease, and the particular peptoids may represent novel small molecule drugs for the treatment of the disease.

5:35 Happy Hour in the Exhibit Hall

6:30 End of Day One


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