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This meeting took place in 2006
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Alzheimer's Disease: Genes, Cellular Pathways and Therapies (J8)
Organizer(s) Rudolph E. Tanzi and Virginia M.-Y. Lee
February 21—26, 2006
Beaver Run Resort • Breckenridge, CO USA
Abstract Deadline: Oct 20, 2005
Late Abstract Deadline: Nov 14, 2005
Scholarship Deadline: Oct 20, 2005
Early Registration Deadline: Dec 21, 2005
Joint Meeting:
Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
Summary of Meeting:
Alzheimer's disease (AD), a progressive neurodegenerative disease, is the most common form of dementia in the elderly. Over the past two decades, studies of AD at the genetic, molecular, and cell biological level have revealed a host of genes, proteins, and biological pathways that impact on the pathogenesis of this disease. Characterization of these pathogenic pathways have suggested several promising therapeutic strategies for treating and preventing AD based on curbing the accumulation of the Abeta peptide in brain, regulating tau hyperphosphorylation, modulating inflammatory responses, and enhancing neurotransmitter function. This meeting will cover updates of the genetics of AD, Abeta generation and clearance pathways, regulation of tau, relevant animal models, novel therapeutic strategies, and advances in imaging and biomarkers for AD diagnosis.
View Scholarships/Awards
Alzheimer's disease (AD), a progressive neurodegenerative disease, is the most common form of dementia in the elderly. Over the past two decades, studies of AD at the genetic, molecular, and cell biological level have revealed a host of genes, proteins, and biological pathways that impact on the pathogenesis of this disease. Characterization of these pathogenic pathways have suggested several promising therapeutic strategies for treating and preventing AD based on curbing the accumulation of the Abeta peptide in brain, regulating tau hyperphosphorylation, modulating inflammatory responses, and enhancing neurotransmitter function. This meeting will cover updates of the genetics of AD, Abeta generation and clearance pathways, regulation of tau, relevant animal models, novel therapeutic strategies, and advances in imaging and biomarkers for AD diagnosis.
View Scholarships/Awards
No registration fees are used to fund entertainment or alcohol at this conference
TUESDAY, FEBRUARY 21
WEDNESDAY, FEBRUARY 22
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
THURSDAY, FEBRUARY 23
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
FRIDAY, FEBRUARY 24
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
SATURDAY, FEBRUARY 25
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
SUNDAY, FEBRUARY 26
Conference Program Print | View meeting in 12 hr (am/pm) time
TUESDAY, FEBRUARY 21
19:30—21:30
Keynote Session (Joint)
*
Rudolph E. Tanzi,
Massachusetts General Hospital, USA
Sangram S. Sisodia,
University of Chicago, USA
Molecular Neurobiology of Alzheimer's Disease
Molecular Neurobiology of Alzheimer's Disease
Cynthia Kenyon,
Calico, USA
Insulin/IGF-1 Signaling, Polyglutamine Aggregation and Aging in C. elegans
Insulin/IGF-1 Signaling, Polyglutamine Aggregation and Aging in C. elegans
*
Jeffery W. Kelly,
The Scripps Research Institute, USA
08:00—11:00
Genetics and Epidemiology of AD
*
Rudolph E. Tanzi,
Massachusetts General Hospital, USA
Steven G. Younkin,
Mayo Clinic Jacksonville, USA
Novel Susceptibility Alleles and Biomarkers for Late Onset AD
Novel Susceptibility Alleles and Biomarkers for Late Onset AD
Mario H. Bengtson,
Genomics Institute of Novartis Foundation, USA
Short Talk: Tauopathy Caused by Mutation of a Novel E3 Ubiquitin Ligase
Short Talk: Tauopathy Caused by Mutation of a Novel E3 Ubiquitin Ligase
Lars Bertram,
Massachusetts General Hospital, USA
The Current Status of Alzheimer's Genetics Research
The Current Status of Alzheimer's Genetics Research
Ellen M. Wijsman,
University of Washington, USA
Complex Models in the Search for Late-onset AD Genes
Complex Models in the Search for Late-onset AD Genes
Lisa A. Paige,
Metabolon Inc., USA
Short Talk: Comparative Metabolomic Analysis of Plasma from Patients with Alzheimer’s Disease or Mild Cognitive Impairment
Short Talk: Comparative Metabolomic Analysis of Plasma from Patients with Alzheimer’s Disease or Mild Cognitive Impairment
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
08:00—11:00
Functional Amyloidogenesis
Susan Lindquist,
HHMI/Whitehead Institute for Biomedical Research, USA
A Yeast Prion Provides a Mechanism for Phenotypic Plasticity
A Yeast Prion Provides a Mechanism for Phenotypic Plasticity
Martijn F.B.G. Gebbink,
University Medical Center Utrecht, Netherlands
Activation of the Contact System and the Fibrinolytic System of Hemostasis by Amyloid Cross-beta Structure
Activation of the Contact System and the Fibrinolytic System of Hemostasis by Amyloid Cross-beta Structure
Douglas M. Fowler,
University of Washington, USA
The Role of Functional Amyloid Formation in Melanogenesis
The Role of Functional Amyloid Formation in Melanogenesis
*
Matthew R. Chapman,
University of Michigan, USA
Protein Misfolding Done Right: The Biogenesis of Bacterial Amyloid Fibers
Protein Misfolding Done Right: The Biogenesis of Bacterial Amyloid Fibers
Yakov A. Vitrenko,
University of Illinois at Chicago, USA
Short Talk: Cross-Seeding between Yeast Sup35 and Rnq1 Prions Involves Formation of Aggregates Containing both Proteins
Short Talk: Cross-Seeding between Yeast Sup35 and Rnq1 Prions Involves Formation of Aggregates Containing both Proteins
17:00—19:00
Amyloid Precursor Protein Function
Sam Gandy,
Mount Sinai Medical Center, USA
Concentration of the Alzheimer Amyloid-beta Precursor Protein In the Neuronal trans-Golgi Network Elevates Abeta42, Mimicking the Effect of Mutant Presenilins
Concentration of the Alzheimer Amyloid-beta Precursor Protein In the Neuronal trans-Golgi Network Elevates Abeta42, Mimicking the Effect of Mutant Presenilins
Roberto Malinow,
University of California, San Diego, USA
AMPA-R: Role in AB induced Loss of Spines
AMPA-R: Role in AB induced Loss of Spines
Thomas C. Südhof,
Stanford School of Medicine, USA
Alpha-Synuclein Cooperates with CSPalpha in Preventing Neurodegeneration
Alpha-Synuclein Cooperates with CSPalpha in Preventing Neurodegeneration
Constanze Reinhard,
Center for Human Genetics, Belgium
Short Talk: Characterization of the sAPP Receptor(s)
Short Talk: Characterization of the sAPP Receptor(s)
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
17:00—19:00
Mechanisms of Amyloidogenesis
Christopher M. Dobson,
University of Cambridge, UK
Protein Folding, Molecular Evolution and Human Disease
Protein Folding, Molecular Evolution and Human Disease
Roland Riek,
The Salk Institute, USA
3D Structures of Amyloid Fibrils of HET-s Prion and Alzheimer Abeta(1-42) fibrils)
3D Structures of Amyloid Fibrils of HET-s Prion and Alzheimer Abeta(1-42) fibrils)
*
David Eisenberg,
University of California, Los Angeles, USA
Crystal Structure Analyses of Amyloid-like Fibrils
Crystal Structure Analyses of Amyloid-like Fibrils
Michael Hecht,
Princeton University, USA
Short Talk: Sequence Determinants of the Aggregation of Alzheimer’s Peptide, Abeta42
Short Talk: Sequence Determinants of the Aggregation of Alzheimer’s Peptide, Abeta42
08:00—11:15
Presenilin and Gamma Secretase
*
Karen Duff,
Columbia University, USA
Dennis J. Selkoe,
Harvard Medical School, USA
The Life Cycle of Amyloid ß-Protein: Mechanisms of Production Synaptotoxicity
The Life Cycle of Amyloid ß-Protein: Mechanisms of Production Synaptotoxicity
Christian Haass,
Ludwig-Maximilians University Munich, Germany
A Common Proteolytic Mechanism For Intramembrane Proteolysis By GxGD-Type Aspartyl Proteases
A Common Proteolytic Mechanism For Intramembrane Proteolysis By GxGD-Type Aspartyl Proteases
Bart De Strooper,
University College London, UK
Genetic and Biochemical Analysis of the Gamma-Secretase Complexes in Mice
Genetic and Biochemical Analysis of the Gamma-Secretase Complexes in Mice
Jie Shen,
Harvard Medical School, USA
Presenilins in Pre- and Post- Synaptic Plasticity and Neurodegeneration
Presenilins in Pre- and Post- Synaptic Plasticity and Neurodegeneration
Homira Behbahani,
Karolinska Institutet, Sweden
Short Talk: Differential Role of Presenilin-1 and -2 on Mitochondrial Membrane Potential and Oxygen Consumption in Mouse Embryonic Fibroblasts
Short Talk: Differential Role of Presenilin-1 and -2 on Mitochondrial Membrane Potential and Oxygen Consumption in Mouse Embryonic Fibroblasts
Taisuke Tomita,
Graduate School of Pharmaceutical Sciences, University of Tokyo, Japan
Short Talk: The Mechanism of gamma-Secretase-Mediated Cleavage Probed by Small Molecule Compounds
Short Talk: The Mechanism of gamma-Secretase-Mediated Cleavage Probed by Small Molecule Compounds
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
08:00—11:00
Protein Folding and Misfolding in Cells and Organisms
William E. Balch,
The Scripps Research Institute, USA
Protein Misfolding and Folding in the Exocytic Pathway
Protein Misfolding and Folding in the Exocytic Pathway
Richard I. Morimoto,
Northwestern University, USA
The Stress of isfolding Proteins: Aging and Neurodegenerative Disease
The Stress of isfolding Proteins: Aging and Neurodegenerative Disease
*
Nancy M. Bonini,
University of Pennsylvania, USA
Human Neurodegenerative Disease: Insights from Drosophila Genetics
Human Neurodegenerative Disease: Insights from Drosophila Genetics
Andrew G. Dillin,
University of California, Berkeley, USA
The Genetics of Aging and Age Related Disease
The Genetics of Aging and Age Related Disease
17:00—19:00
Beta-Secretase
*
Dennis J. Selkoe,
Harvard Medical School, USA
Donald L. Price,
Johns Hopkins University, USA
Neurodegenerative Diseases: Models, Mechanisms and Experimental Therapeutics
Neurodegenerative Diseases: Models, Mechanisms and Experimental Therapeutics
Jordan J. Tang,
Oklahoma Medical Research Foundation, USA
Cellular Trafficking of Memapsin 2 and APP Mediated by Protein Factors
Cellular Trafficking of Memapsin 2 and APP Mediated by Protein Factors
Edward B. Lee,
Hospital of the University of Pennsylvania, USA
BACE Activity and the Subcellular Localization of APP Cleavage
BACE Activity and the Subcellular Localization of APP Cleavage
Michael Willem,
Adolf-Butenandt-Institute, Germany
Short Talk: Functional Analysis of BACE1
Short Talk: Functional Analysis of BACE1
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
17:00—19:00
Therapeutic Strategies Towards Misfolding Diseases
Jeffery W. Kelly,
The Scripps Research Institute, USA
Towards Understanding and Ameliorating Protein Misfolding Disease
Towards Understanding and Ameliorating Protein Misfolding Disease
Michel Bouvier,
University of Montreal, Canada
Molecular Mechanisms of Action and Therapeutic Potential of Pharmacological Chaperones on Misfolded G Protein-Coupled Receptors
Molecular Mechanisms of Action and Therapeutic Potential of Pharmacological Chaperones on Misfolded G Protein-Coupled Receptors
*
Leslie M. Thompson,
University of California, Irvine, USA
Therapeutic Strategies for Huntington’s Disease
Therapeutic Strategies for Huntington’s Disease
Aaron D. Gitler,
Stanford University School of Medicine, USA
Short Talk: Alpha-Synuclein Toxicity Involves Inhibition of Endoplasmic Reticulum (ER) to Golgi Trafficking
Short Talk: Alpha-Synuclein Toxicity Involves Inhibition of Endoplasmic Reticulum (ER) to Golgi Trafficking
08:00—11:15
Tau and FTD
Lester I. Binder,
Northwestern University, USA
Tau Alterations in Alzheimer's Disease
Tau Alterations in Alzheimer's Disease
Karen Duff,
Columbia University, USA
Phosphorylation as a Pathogenic Mechanism in AD
Phosphorylation as a Pathogenic Mechanism in AD
Eva-Maria Mandelkow,
Max Planck Institut, Germany
The Modes and Pathways of Tau's Toxicity to Neurons in Neurodegeneration
The Modes and Pathways of Tau's Toxicity to Neurons in Neurodegeneration
Michael Hutton,
Eli Lilly Research Center, UK
Genetics of the Tauopathies
Genetics of the Tauopathies
Chad A. Dickey,
University of South Florida, USA
Short Talk: Deletion of CHIP Leads to Caspase-3 Activation and Neuronal Apoptosis Associated with Increases in Non-Ubiquitinated, Soluble Phospho-Tau Species without Neurofibrillary Tangles
Short Talk: Deletion of CHIP Leads to Caspase-3 Activation and Neuronal Apoptosis Associated with Increases in Non-Ubiquitinated, Soluble Phospho-Tau Species without Neurofibrillary Tangles
Kun Ping Lu,
Beth Israel Deaconess Medical Center, USA
Short Talk: The Isomerase Pin1: a Potential New Link between Tangle and Plaque Pathologies of Alzheimer’s Disease
Short Talk: The Isomerase Pin1: a Potential New Link between Tangle and Plaque Pathologies of Alzheimer’s Disease
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
08:00—11:00
Cellular Mechanisms for Handling Misfolded Proteins
Eva-Maria Mandelkow,
Max Planck Institut, Germany
Tau Protein Structure and Aggregation
Tau Protein Structure and Aggregation
*
Randy Y. Hampton,
University of California, San Diego, USA
ERAD as a Strategy of Protein Quantity Control
ERAD as a Strategy of Protein Quantity Control
Jonathan S. Weissman,
Whitehead Institute and MIT, USA
A Novel Branch of the Unfolded Protein Response
A Novel Branch of the Unfolded Protein Response
Randal J. Kaufman,
Sanford-Burnham Medical Research Institute, USA
The Unfolded Protein Response: A Link between ER Stress and Inflammation
The Unfolded Protein Response: A Link between ER Stress and Inflammation
17:00—19:00
Abeta Clearance
*
Cynthia A. Lemere,
Brigham and Women's Hospital, Harvard Medical School, USA
David M. Holtzman,
Washington University, USA
Effects of ApoE Levels, Isoform, and Lipidation on CNS Abeta Clearance and Fibrillogenesis
Effects of ApoE Levels, Isoform, and Lipidation on CNS Abeta Clearance and Fibrillogenesis
Berislav Zlokovic,
University of Southern California, USA
Neurovascular Mechanisms and Targets in AD
Neurovascular Mechanisms and Targets in AD
Louis B. Hersh,
University of Kentucky, USA
AB Degrading Peptidases
AB Degrading Peptidases
Matthew Townsend,
Brigham and Women's Hospital, USA
Short Talk: The Cyclohexanehexol, AZD-103, Neutralizes Cell-derived ABeta Oligomers and Rescues Hippocampal Long-Term Potentiation
Short Talk: The Cyclohexanehexol, AZD-103, Neutralizes Cell-derived ABeta Oligomers and Rescues Hippocampal Long-Term Potentiation
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
17:00—19:00
The Response to Damaged Proteins
Paul Wentworth, Jr.,
The Scripps Research Institute, USA
Oxidative Metabolite Triggered Protein Misfolding
Oxidative Metabolite Triggered Protein Misfolding
Ana Maria Cuervo,
Albert Einstein College of Medicine, USA
Autophagy in Aging: The Importance of Maintaining Cells Clean
Autophagy in Aging: The Importance of Maintaining Cells Clean
Claudio A. Hetz,
University of Chile, Chile
Short Talk: Proapoptotic BAX and BAK Modulate the Unfolded Protein Response through a Direct Interaction with Ire1alpha
Short Talk: Proapoptotic BAX and BAK Modulate the Unfolded Protein Response through a Direct Interaction with Ire1alpha
08:00—11:15
Animal Models and Therapeutics
*
Sam Gandy,
Mount Sinai Medical Center, USA
Cynthia A. Lemere,
Brigham and Women's Hospital, Harvard Medical School, USA
Modulating the Immune Response in Abeta Immunotherapy
Modulating the Immune Response in Abeta Immunotherapy
Charles G. Glabe,
University of California, Irvine, USA
Immunization of transgenic mouse models of degenerative disease against amyloid oligomers.
Immunization of transgenic mouse models of degenerative disease against amyloid oligomers.
Dora M. Kovacs,
Massachusetts General Hospital, USA
Cholesterol-Related AD Therapeutics
Cholesterol-Related AD Therapeutics
Abraham Fisher,
Israel Institute for Biological Research, Israel
M1 Muscarinic Agonists - Promising Agents on Major Hallmarks of Alzheimer's Disease
M1 Muscarinic Agonists - Promising Agents on Major Hallmarks of Alzheimer's Disease
Steven E. Jacobsen,
University of California, Los Angeles, USA
Short Talk: Preclincal and Behavioral Models of Alzheimer’s Disease Passive Immunotherapy
Short Talk: Preclincal and Behavioral Models of Alzheimer’s Disease Passive Immunotherapy
Thomas A. Bayer,
University of Saarland, Germany
Short Talk: Intraneuronal Aß, Neuron Loss and Axonopathy in Transgenic Mouse Models for Alzheimer's Disease
Short Talk: Intraneuronal Aß, Neuron Loss and Axonopathy in Transgenic Mouse Models for Alzheimer's Disease
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
08:00—09:30
Emerging Misfolding Diseases
Gunilla T. Westermark,
Linköping University, Sweden
Islet Amyloid and Beta Cell Destruction in Diabetes
Islet Amyloid and Beta Cell Destruction in Diabetes
Marina Ramirez-Alvarado,
Mayo Clinic College of Medicine, USA
Light Chain Amyloidosis-When Elevated Amounts of Protein, Multiple Mutations, Proteolytic Cleavage, and Loss of Associations Come Together
Light Chain Amyloidosis-When Elevated Amounts of Protein, Multiple Mutations, Proteolytic Cleavage, and Loss of Associations Come Together
Matthew J. Trifilo,
The Scripps Research Institute, USA
Short Talk: Conversion of PrPsen to PrPres and Extraneural Disease Associated with Amyloidogenic PrPres Deposits Occur in the Absence of PrP’s GPI Anchor
Short Talk: Conversion of PrPsen to PrPres and Extraneural Disease Associated with Amyloidogenic PrPres Deposits Occur in the Absence of PrP’s GPI Anchor
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
09:50—11:00
Organismal Models of Protein Misfolding Diseases
*
Marie-Francoise Chesselet,
University of California, Los Angeles, USA
Mouse Models of Parkinson’s and Huntington’s Disease
Mouse Models of Parkinson’s and Huntington’s Disease
Don W. Cleveland,
University of California, San Diego, USA
From Charcot to Lou Gehrig: The Unfolding Story in Mechanism and Treatment of ALS
From Charcot to Lou Gehrig: The Unfolding Story in Mechanism and Treatment of ALS
17:00—19:00
Therapeutics and Imaging
*
Charles G. Glabe,
University of California, Irvine, USA
Edward Koo,
University of California, San Diego, USA
APP Function and Effects of NSAIDs
APP Function and Effects of NSAIDs
Christoph Hock,
University of Zurich, Switzerland
Biomarkers for Alzheimer's Disease
Biomarkers for Alzheimer's Disease
Chester Mathis,
UPMC Presbyterian Hospital, USA
Imaging beta-Amyloid in vivo
Imaging beta-Amyloid in vivo
Ward Pedersen,
Creighton University Medical Center, USA
Short Talk: Rosiglitazone Attenuates Glucocorticoid-Induced Learning and Memory Deficits in Tg2576 Alzheimer Mice
Short Talk: Rosiglitazone Attenuates Glucocorticoid-Induced Learning and Memory Deficits in Tg2576 Alzheimer Mice
Following Session is for Protein Misfolding Diseases: Mechanisms of Misfolding, Pathology and Therapeutic Strategies (J7)
17:00—19:00
Emerging Topics Session: Short Talks Selected from Abstracts
*
Matthew J. Trifilo,
The Scripps Research Institute, USA
Abraham Grossman,
Q-RNA.com, USA
Small RNA Chaperones Facilitate Amyloid Protein Transformation in vitro and Lead to Aggregate Formation and Behavior Abnormalities in Drosophila
Small RNA Chaperones Facilitate Amyloid Protein Transformation in vitro and Lead to Aggregate Formation and Behavior Abnormalities in Drosophila
Christopher D. Link,
University of Colorado, USA
Cellular Toxicity of Aggregating Proteins
Cellular Toxicity of Aggregating Proteins
Soumya S. Ray,
Schrödinger, USA
Designing Aggregation Inhibitors of Superoxide Dismutase Mutants Linked to ALS
Designing Aggregation Inhibitors of Superoxide Dismutase Mutants Linked to ALS
Leila M. Luheshi,
University of Cambridge, UK
Can we Predict the in Vivo Aggregation and Toxicity of AB 1-42 Mutants From their Intrinsic Aggregation Propensities?
Can we Predict the in Vivo Aggregation and Toxicity of AB 1-42 Mutants From their Intrinsic Aggregation Propensities?
Shohei Koide,
New York University Langone Health, USA
Short Talk: High Resolution Structures of Peptide Self-Assemblers
Short Talk: High Resolution Structures of Peptide Self-Assemblers
Rajaraman Krishnan,
Proclara Biosciences, USA
Short Talk: Structural Insights on a Yeast Prion Illuminate Necleation and Strain Diversity
Short Talk: Structural Insights on a Yeast Prion Illuminate Necleation and Strain Diversity
Jessie Chu,
The Scripps Research Institute, USA
Short Talk: A Novel E3 Ubiquitin Ligase Involvd in Neurodegeneration
Short Talk: A Novel E3 Ubiquitin Ligase Involvd in Neurodegeneration
*Session Chair †Invited, not yet responded.
We gratefully acknowledge the generous grant for this conference provided by:
We gratefully acknowledge additional support for this conference from:
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Alzheimer's Association |
rPeptide, LLC |
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