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James Lah, M.D., Ph.D.
Emory University
Atlanta, GA
Title:
Targeted Discovery of LR11/SorLA-Based AD Therapeutics
Non-Technical Title:
Drug Discovery for Alzheimer's Disease
Duration:
April 1, 2007 - March 31, 2010
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Summary: We propose to initiate a search for LR11-interacting compounds, which will produce leads in the development of new therapeutic agents. To accomplish this, we will combine our scientific expertise with the capabilities of the NIH-funded Emory Molecular Libraries Screening Center to develop tools to identify and evaluate candidate compounds that interact with LR11.
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Program: Alzheimer's Disease
Award Type: Standard
$300,000
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Bruce Lamb, Ph.D.
The Cleveland Clinic Foundation
Cleveland, OH
Title:
Microglia , CX3CR1and Alzheimer's Disease Pathogenesis
Non-Technical Title:
Activation of the immune system in AD
Duration:
April 1, 2007 - March 31, 2010
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Summary: The focus of the current proposal is to determine the role of CX3CR1 plays in activation of the immune system, neuronal cell death and Aß deposition in two different mouse models of AD as well as to gain insight into the mechanisms involved. The long-term goal of this project is to gain insight into the role inflammation play in AD and thus provide potential new avenues of therapeutic intervention.
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Program: Alzheimer's Disease
Award Type: Standard
$400,000
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Malcolm Leissring, Ph.D.
Mayo Clinic Jacksonville
Jacksonville, FL
Title:
Catabolism Of Amyloid Beta And Tau By Cathepsin D In Vivo
Non-Technical Title:
Can Alzheimer Disease Be Treated With The Enzyme Cathepsin D?
Duration:
April 1, 2009 - March 31, 2012
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Summary: We have discovered that deletion of an enzyme known as cathepsin D (CatD) in mice results in very large and very selective increases in the two toxic protein species that are most closely linked to two characteristics of Alzheimer's disease (AD): (1) the amyloid beta-protein (specifically the 42-amino acid form, amyloid beta42), which deposits in the extracellular "plaques" that characterize AD, and (2) the microtubule-associated protein, tau, which makes up the neurofibrillary tangles that form inside neurons in AD and other diseases. We hypothesize that CatD plays a protective role in preventing AD by (directly or indirectly) breaking down amyloid beta42 and tau. We will test this hypothesis by increasing or decreasing CatD levels in mice that accumulate either amyloid beta 42 or tau.
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Program: Alzheimer's Disease
Award Type: Standard
$400,000
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Alan Lerner, M.D.
University Hospitals of Cleveland
Cleveland, OH
Title:
Teen IQ, Activity Level, and AD: Mechanisms of the Links
Non-Technical Title:
Duration:
April 1, 2006 - March 31, 2010
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Summary:
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Program: Alzheimer's Disease
Award Type: Pilot
$85,500
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Rena Li, Ph.D.
Sun Health Research Institute
Sun City, AZ
Title:
Estrogen And Its Receptors In BACE1 Regulation: From Cells To Mice
Non-Technical Title:
Estrogen In Alzheimer’s Disease
Duration:
April 1, 2009 - March 31, 2012
Co-Investigator(s):
Yong Shen, M.D., Ph.D.
Sun Health Research Institute
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Summary: Reduction of estrogen in postmenopausal women might cause a higher risk of developing Alzheimer's disease (AD). Studies show that inhibition of beta-secretase (BACE1) might play a major role in preventing AD. Our study on estrogen and estrogen receptors in BACE1 regulation will not only provide better understanding of molecular mechanisms of estrogen in preventing AD, but also provide scientific evidence for new drug development.
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Program: Alzheimer's Disease
Award Type: Standard
$399,761
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Dezhi Liao, Ph.D.
University of Minnesota
Minneapolis, MN
Title:
Abnormal Presence Of Tau Proteins In Dendritic Spines
Non-Technical Title:
Tau In A Wrong Place
Duration:
April 1, 2009 - March 31, 2011
Co-Investigator(s):
Karen Hsiao Ashe, M.D., Ph.D.
University of Minnesota
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Summary: We will test the novel concept that specific chemical modification drives unual targeting of Alzheimer’s-linked “tau” proteins to the dendritic spines of neurons. This targeting might provide a mechanistic link between amyloid and tauopathies, hallmarks of the Alzheimer’s disease (AD) process. Therefore, the successful completion of this project will provide a more complete mechanistic model for AD than available at present.
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Program: Alzheimer's Disease
Award Type: Pilot
$150,000
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Paul Lombroso, M.D.
Yale University
New Haven, CT
Title:
The Role of STEP in Alzheimer's Disease
Non-Technical Title:
New Targets for the Treatment of Alzheimer's Disease
Duration:
April 1, 2008 - March 31, 2011
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Summary: By using transgenic animal models of Alzheimer's disease, this project seeks to test whether slowing down the activity of a particular molecular pathway can restore cognitive abilities.
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Program: Alzheimer's Disease
Award Type: Standard
$400,000
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Kun-Ping Lu, M.D., Ph.D.
Beth Israel Deaconess Medical Center
Boston, MA
Title:
Role of Pin1 and Presenilin-1 Interaction In Vivo
Non-Technical Title:
Regulating production of ABeta
Duration:
April 1, 2007 - September 30, 2009
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Summary: Our hypothesis in this proposal is that Pin1 might also regulate the function of presenilin 1, an essential component of the enzyme responsible for ABeta production, and that this regulation might be disrupted by some Alzheimer’s mutations in presenilin 1. To test this hypothesis, we will determine whether Pin1 regulates presenilin 1 structure in a test tube, whether manipulating Pin1 function affects PS1 activity in cell culture and animal models, and whether this Pin1-dependent regulation is disrupted by presenilin 1 mutations.
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Program: Alzheimer's Disease
Award Type: Pilot
$150,000
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Mathias Lösche, Ph.D.
Carnegie Mellon University
Pittsburgh, PA
Title:
Lipid Bilayer Reorganization by Amyloid-beta Oligomers
Non-Technical Title:
How do misfolded peptide aggregates affect neuronal cell membranes?
Duration:
April 1, 2008 - March 31, 2010
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Summary: This team will use synthetic models of neuronal cell membranes, to study how ABeta interacts with these membranes. The results of these studies will be insight into the damaging effects of ABeta and how this effect varies with membrane lipid composition.
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Program: Alzheimer's Disease
Award Type: Pilot
$149,940
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Cynthia Massaad, Ph.D.
Baylor College of Medicine
Houston, TX
Title:
The Role of Mitochondrial Superoxide in Alzheimer's Pathology
Non-Technical Title:
Identifying a novel antioxidant target for Alzheimer's disease therapy
Duration:
April 1, 2008 - October 31, 2010
Mentor:
Robia Pautler, Ph.D.
Baylor College of Medicine
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Summary: This project examines the role of antioxidants in mouse models of Alzheimer's disease. The study will examine the pathophysiological basis of the disease using Magnetic Resonance Imaging (MRI). The outcomes of this project will predict ways of using antioxidant therapy to overcome Alzheimer's disease.
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Program: Alzheimer's Disease
Award Type: Research Fellowship
$100,000
