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Thursday, June 17
7:30 - 8:20 am BREAKOUT DISCUSSION
Challenging Hypotheses for Alzheimer's Disease
Small working groups will challenge current hypotheses for targeting Alzheimer's disease, including addressing the following questions:
- What data do we need to disprove the amyloid hypothesis?
- Is there room for more than one right answer?
Moderator: William J. Ray, Ph.D., Director, Neurology, Merck Research Laboratories
8:20 Chairperson's Remarks
Cornelia Reininger, M.D., Ph.D., Director, Global Clinical Development, Bayer Health Care Pharmaceuticals
8:30 Imaging of Alzheimer’s Disease: a Drug Discovery and Development Perspective
Thomas Krucker, Ph.D., Head, Molecular Imaging, Novartis Institute for Biomedical Research
Genetically modified mice modeling Alzheimer’s disease enable the study of disease progression, determine early diagnosis, and test potential therapeutic interventions. Exploring new concepts and imaging strategies allowed us to successfully monitor non-invasively amyloid deposition, a hallmark of Alzheimer’s disease, using novel probe technology. Although challenging, translation of such strategies into clinical applications have great potential. Various approaches, possible alternatives and limitations will be discussed.
9:00 The Role of Amyloid Tracers in: Disease Detection in AD, Early Identification and Pre-Selection for Therapy
Cornelia Reininger, M.D., Ph.D., Director, Global Clinical Development, Bayer Health Care Pharmaceuticals
9:30 Preclinical Imaging of Amyloid-BETA Plaque: In Search of an Animal Model
Cyrille Sur, Ph.D., Director, Molecular Imaging, Merck Research Laboratories
The deposition of amyloid-BETA (ABETA) plaque in the brain is a hallmark of Alzheimer's Disease (AD). Brain ABETA deposits can be imaged in AD patients with specific positron emission tomography tracers such as [11C]PIB and [18F]AV-45. Yet, ABETA plaque imaging in preclinical animal models has not been successful and I will present results from the evaluation of various technologies and animal models.
10:00 Networking Coffee Break, Poster and Exhibit Viewing
10:40 Chairperson's Remarks
Carol A. Colton, Ph.D., Professor, Neurology, Duke University
10:45 Developing New Targets for Alzheimer's Disease Using Functional Genomics
William J. Ray, Ph.D., Director, Neurology, Merck Research Laboratories
The disease-associated genes identified thus far have led to attractive hypotheses regarding specific biological processes that could drive disease progression, but have been challenging to develop as drug targets. We are using high throughput genomics to identify genes that modulate the same disease-relevant biological processes but are amenable to pharmacology with the hopes of addressing fundamental questions in patients.
11:15 Metabolic Targets for Alzheimer Disease
Mark A. Smith, Ph.D., Professor of Pathology, Case Western Reserve
Metabolic dysfunction and oxidative stress are early and pervasive mediators of neurodegeneration in Alzheimer disease. Since it is apparent that abnormal mitochondrial and hormonal imbalances are crucial mediators, stabilizing metabolic dysfunction provides a potential therapeutic opportunity for intervention. In this presentation, recent preclinical and clinical trial data on agents that target metabolic aspects of disease will be discussed.
11:45 Luncheon Presentations (Sponsorship Opportunities Available) or Lunch on Your Own
1:15 pm Chairperson's Remarks
1:25 GAMMA-Secretase as a Target for Alzheimer Disease Therapy: Small Molecule Development
Corinne E. Augelli-Szafran, Ph.D., Director, Laboratory for Experimental Alzheimer Drugs (LEAD), Brigham and Women's Hospital, Center for Neurologic Diseases and Harvard Medical School, Department of Neurology
LEAD, an academic drug discovery laboratory, is currently focused on the identification of -secretase modulators that lower ABETA production and leave Notch signaling intact. Through iterative design, synthesis, and pharmacological evaluation of more than 900 small molecules, approximately 10% have these characteristics. An overview of LEAD’s program and the current status of key lead compounds will be presented.
1:55 a7 Nicotinic Acetylcholine Receptor Agonists: Therapeutic Promise for Symptomatic and Disease Modifying Efficacy in Alzheimer’s Disease
Timothy A. Esbenshade, Ph.D., Senior Group Leader, Associate Fellow, Neuroscience Research, Abbott Laboratories
Nicotinic acetylcholine receptors (nAChRs) are localized in brain regions associated with cognition and modulate the release of neurotransmitters that play important roles in cognitive processes. a7 nicotinic acetylcholine receptor (nAChR) agonists are efficacious in preclinical cognition models and neuroprotective signaling pathways associated with Alzheimer’s disease (AD). This presentation will review the current understanding of the neurobiological function of a7 nAChRs in modulating neurotransmitter release, cognitive processes, and neuroprotection as well as discuss the therapeutic potential of a7 nAChR agonists for the treatment of AD.
2:25 Ice Cream Refreshment Break in the Exhibit Hall
3:05 EXPERT PANEL
Bridging the Gap Between Alzheimer’s Disease Research and Drug Discovery: What are the Key Features for Moving a Compound Forward?
Moderator: Corinne E. Augelli-Szafran, Ph.D., Director, Laboratory for Experimental Alzheimer Drugs (LEAD), Brigham and Women’s Hospital, Center for Neurologic Diseases and Harvard Medical School, Department of Neurology
Panelists:
William J. Ray, Ph.D., Director, Neurology, Merck Research Laboratories
Mark A. Smith, Ph.D., Professor of Pathology, Case Western Reserve
Carol A. Colton, Ph.D., Professor, Neurology, Duke University
3:35 Development of Novel HDAC Inhibitors for Neurodegenerative Diseases
Holger Patzke, Ph.D, Associate Director, EnVivo Pharmaceuticals
Epigenetic mechanisms may account for observed pathologic transcriptional aberrations in CNS disease. In order to counter these transcriptional disturbances, we have developed novel, orally bioavailable and CNS penetrant HDAC inhibitors. This presentation will describe the discovery of EVP-0334, an HDAC inhibitor that exhibits pro-cognitive activity and may have utility in several CNS diseases, including AD.
4:05 Targeting Glia-Neuron Interactions That Result in Synaptic Dysfunction as a Drug Discovery Strategy for Alzheimer’s Disease
Linda VanEldik, Ph.D., Director, Sanders-Brown Center on Aging, and Professor, Department of Anatomy and Neurobiology, University of Kentucky, Lexington KY
A discovery engine for development of selective, efficacious, blood-brain-barrier penetrant, novel small molecules that modulate key intracellular signaling pathways has yielded new potential disease- modifying therapeutic candidates. The talk will focus on two compound classes that have different molecular targets and are efficacious in animal models of CNS disorders, attenuating the overproduction of proinflammatory cytokines and synaptic dysfunction.
4:35 End of Conference
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