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J. Kevin Foskett, Ph.D.
University of Pennsylvania
Philadelphia, PA
Title:
IP3R-Presenilin Interaction: Calcium Dysregulation in AD
Non-Technical Title:
Calcium disruption in Alzheimer's Disease
Duration:
April 1, 2008 - March 31, 2011
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Summary: This study is designed to test how presenilin interacts with calcium signaling proteins, resulting in changes to the presenilin function. The study will also examine how altered calcium signaling in turn affects other cell functions. These studies should provide new insights into the molecular mechanisms of AD and into the development of novel targets for therapeutic interventions.
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Program: Alzheimer's Disease
Award Type: Standard
$400,000
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Alison Goate, D.Phil.
Washington University
St. Louis, MO
Title:
Identification of functional alleles that influence cerebrospinal fluid levels of Aß and risk for Alzheimer's disease
Non-Technical Title:
Searching for genetic variation that influences cerebrospinal fluid protein levels and risk for Alzheimer's disease
Duration:
April 1, 2008 - March 31, 2011
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Summary: Comparisons of levels of A Beta peptides found in the cerebrospinal fluid can be used to predict the risk of developing Alzheimer's disease. By searching for genes that perturb the ratios of ABeta levels in the CSF this proposal seeks to identify new genes involved in the development of late onset Alzheimer's disease.
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Program: Alzheimer's Disease
Award Type: Standard
$400,000
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Francine Grodstein, Sc.D.
Harvard University
Boston, MA
Title:
Mid-life Telomere Length and Cognitive Decline in Later Life
Non-Technical Title:
Markers of Aging at Mid-life and Memory at Older Ages
Duration:
April 1, 2008 - September 30, 2010
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Summary: Previous studies have provided suggestive evidence for an association between telomere length and cognitive function. This study aims determine whether telomere length might predict status of cognitive decline 10 years later by analyzing data from the Nurses' Health Study.
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Program: Alzheimer's Disease
Award Type: Pilot
$100,000
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Zhefeng Guo, Ph.D.
University of California, Los Angeles
Los Angeles, CA
Title:
EPR studies of the structures of Abeta oligomers
Non-Technical Title:
Mechanisms of neurotoxicity in Alzheimer's disease
Duration:
April 1, 2010 - March 31, 2012
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Summary: Recent studies suggest that amyloid beta oligomers, or aggregation of only a few amyloid beta molecules, are the primary toxic species in the development of Alzheimer's disease. In this project, we will study the structures of two amyloid beta oligomers with electron paramagnetic resonance (EPR) spectroscopy. This work will help understand the structural basis of neurotoxicity of amyloid beta oligomers and guide the development of new therapeutic strategies.
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Program: Alzheimer's Disease
Award Type: Pilot
$150,000
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Byung Hee Han, Ph.D.
Washington University
Saint Louis, MO
Title:
PET tracers for cerebrovascular-specific amyloid imaging
Non-Technical Title:
Non-invasive imaging agents for cerebrovascular amyloid deposition
Duration:
April 1, 2010 - March 31, 2012
Co-Investigator(s):
Robert Mach,
Washington University
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Summary: Cerebral amyloid angiopathy (CAA) is a common blood vessel disorder in the elderly and associated with vascular deposition of fibrillar amyloid beta (ABeta), which is also found in the neuritic plaques of patients with Alzheimer's disease (AD). Though ABeta imaging tracers have been designed to identify ABeta deposits in AD patients, available tracers non-selectively bind both CAA and neuritic plaques. Thus the “background” from tracers that bind neuritic plaques reduces the ability of clinicians and researchers to visualize ABeta that binds to CAA. Results from this research project may lead to development of a unique CAA-selective amyloid tracer that would permit definitive diagnosis of CAA in living patients.
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Program: Alzheimer's Disease
Award Type: Pilot
$150,000
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Jeremy Herskowitz, Ph.D.
Emory University
Atlanta, GA
Title:
The role of LR11 intracellular traffic in Alzheimer's disease
Non-Technical Title:
Protein traffic: the disease-causing mechanism of Alzheimer's disease?
Duration:
April 1, 2010 - March 31, 2012
Mentor:
James Lah, M.D., Ph.D.
Emory University
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Summary: There are no known therapies for the underlying disease-causing mechanisms of Alzheimer's disease, the leading cause of dementia. The study of LR11, also known as SorLA, a pathogenic factor with multiple influences on Alzheimer's disease susceptibility, will bolster our knowledge of the underlying cellular mechanisms by which LR11 may influence the onset and progress of Alzheimer's disease.
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Program: Alzheimer's Disease
Award Type: Research Fellowship
$100,000
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Joachim Herz, M.D.
The University of Texas Southwestern Medical Center at Dallas
Dallas, TX
Title:
An Apoe Receptor-Mediated Mechanism For AD Pathogenesis
Non-Technical Title:
Apoe Receptors In Alzheimer's Disease
Duration:
April 1, 2009 - March 31, 2012
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Summary: We have identified a novel conceptual mechanism by which ApoE and amyloid beta peptide interact at the level of the synapse. This mechanism has the potential to explain the fundamental molecular pathways that underlie the causes of Alzheimer's disease. Understanding of these mechanisms may open a new door to effective, rational drugs designed to work against Alzheimer's disease.
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Program: Alzheimer's Disease
Award Type: Standard
$400,000
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George Jackson, M.D., Ph.D.
University of Texas Medical Branch
Galveston, TX
Title:
Validation and Characterization of Tau Modifiers In Vivo
Non-Technical Title:
Examining regulation of tau protein
Duration:
April 1, 2007 - August 31, 2010
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Summary: These experiments propose further studies of the role of PSA in tauopathy, and plan to validate other genes identified as putative protective or susceptibility genes in the transgenic human tau P301L mouse model.
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Program: Alzheimer's Disease
Award Type: Standard
$400,000
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Joanna Jankowsky, Ph.D.
Baylor College of Medicine
Houston, TX
Title:
Separating cell-autonomous from -extrinsic effects of APP/Ab
Non-Technical Title:
Murder or suicide - how does APP/Amyloid beta cause neuronal dysfunction?
Duration:
April 1, 2010 - March 31, 2013
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Summary: The amyloid precursor protein and its derivative, amyloid beta, are intimately associated with the onset and progression of Alzheimer's, yet there are still many basic questions about their role in neuronal dysfunction that remain unanswered because we lack appropriate model systems in which to address them. We are investigating a new “viral mosaic APP” transgenic mouse model that allows us to tackle fundamental questions about whether APP and amyloid beta act locally in a single cell or exert their effects between cells to alter neuronal structure and function. We are exploring whether their overexpression in the mature brain has distinct effects from those effects that might be seen during early embryological and post-natal development. Answers to these deceptively basic questions will be critical to understanding how APP/amyloid beta contributes to Alzheimer's pathogenesis and determine how best to target its action therapeutically.
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Program: Alzheimer's Disease
Award Type: Standard
$396,504
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Thomas Jongens, Ph.D.
The Trustees of the University of Pennsylvania
Philadelphia, PA
Title:
Testing For Calcium Dysregulation In A New AD Model
Non-Technical Title:
Determining If Calcium Levels Are Linked To Loss Of Mental Abilities
Duration:
April 1, 2009 - March 31, 2011
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Summary: One hypothesis, put forth by several investigators, is that dysregulation of intracellular calcium is an early or central cause of at least some of the symptoms of Alzheimer's disease. In the experiments outlined in this proposal we will determine if the misregulation of intracellular calcium levels is linked to the age of onset of cognitive deficits that we observe in a new Drosophila (fruit fly) model for Alzheimer's disease that is based on loss of presenilin activity.
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Program: Alzheimer's Disease
Award Type: Pilot
$150,000
