|
Paul Salvaterra, Ph.D.
Beckman Research Institute of the City of Hope
Duarte, CA
Title:
Ab and Neurodegeneration
Non-Technical Title:
Ab and neurodegeneration
Duration:
April 1, 2007 - March 31, 2011
|
Summary: Our work is designed to investigate the role of certain peptides, both alone and in combination, as direct causes of chronic brain cell death. We will accomplish this by using a simplified genetically controlled model organism. We also believe that our preliminary observations indicate a new cellular pathway that may be responsible for Alzheimer's related cell death. We will thus try and prove this hypothesis using genetic and drug based experimental strategies in our model system.
More details
Program: Alzheimer's Disease
Award Type: Standard
$400,000
|
Jakob Satz, Ph.D.
The Jackson Laboratory
Bar Harbor, ME
Title:
Protective role of Stim in neurodegenerative disease
Non-Technical Title:
Suppression of Plaques and Tangles by a Novel Modifier Gene
Duration:
April 1, 2010 - March 31, 2012
Mentor:
Susan Ackerman,
The Jackson Laboratory
|
Summary: Plaques and tangles are accumulations of misfolded proteins that form in Alzheimer's disease. These protein aggregates are thought to be toxic to cells in the brain. We have identified a modifier gene that suppresses aggregation of many misfolded proteins. This project outlines experiments to study how this modifier works, and to test its ability to suppress the accumulation of plaques and tangles in animal models of Alzheimer's disease.
More details
Program: Alzheimer's Disease
Award Type: Research Fellowship
$100,000
|
|
Vijay Sharma, Ph.D.
Washington University
St. Louis, MO
Title:
Imaging PGP-Mediated Transport in Alzheimer's Disease
Non-Technical Title:
Improving imaging tools for diagnosis of AD
Duration:
April 1, 2007 - September 30, 2010
|
Summary: We propose to evaluate the potential of lead Pgp-targeted agent to act as noninvasive probe to detect those defects in brains of mouse models via PET imaging. Additionally, our strategy is amenable to kit formulation with potential for widespread deployment of a test for managing AD.
More details
Program: Alzheimer's Disease
Award Type: Pilot
$150,000
|
|
Gerry Shaw, Ph.D.
University of Florida
Gainesville, FL
Title:
Blood And CSF Biomarkers Of Alzheimer's Disease
Non-Technical Title:
Monitoring Alzheimer's Disease
Duration:
April 1, 2009 - March 31, 2011
|
Summary: Alzheimer's disease is difficult to diagnose and it is also difficult to monitor the progression of the disease. We have developed two assays which can be used to monitor neurodegeneration using blood and cerebrospinal fluid (CSF) samples. The aim of the present proposal is to see if these assays can be used to monitor Alzheimer's disease.
More details
Program: Alzheimer's Disease
Award Type: Pilot
$150,000
|
|
Reisa Sperling, M.D.
Brigham and Women's Hospital
Boston, MA
Title:
Cholinergic Vulnerability in Amyloid-Positive Elderly
Non-Technical Title:
Susceptibility to drug-induced memory impairment in older subjects with amyloid
Duration:
April 1, 2010 - March 31, 2013
|
Summary: This study will use a "scopolamine stress test" to test the hypothesis that older individuals harboring hidden amyloid pathology, as identified through brain imaging, are more vulnerable to the effects of the stress test on memory performance and functional MRI measures of memory network activity.
More details
Program: Alzheimer's Disease
Award Type: Standard
$399,143
|
|
Grace Stutzmann, Ph.D.
Rosalind Franklin University / The Chicago Medical School
North Chicago, IL
Title:
Targeting aberrant calcium signaling for Alzheimer’s Disease therapeutics
Non-Technical Title:
Normalizing neuronal function in Alzheimer’s disease using calcium channel blockers
Duration:
April 1, 2010 - March 31, 2012
|
Summary: The broad question this project is designed to address is what is the functional relationship between calcium dysregulation in Alzheimer’s disease and the hallmark features of the disease. As a breakdown in synaptic function and structure is correlated most highly with cognitive loss, this aspect will be a significant focus. If Ryanodine receptor (RyR)-mediated calcium release is intimately involved in Alzheimer’s disease pathogenesis in both early and late stages, then manipulating RYR ion channel function should offer both novel therapeutic strategies, and, a better understanding of the disease process itself.
More details
Program: Alzheimer's Disease
Award Type: Pilot
$150,000
|
|
Jaehong Suh, Ph.D.
Massachusetts General Hospital
Charlestown, MA
Title:
Effect of Novel Alzheimer’s diseaseAM10 Gene Mutations in Alzheimer's Disease
Non-Technical Title:
Mutations in the Alzheimer’s diseaseAM10 gene can cause Alzheimer's disease
Duration:
April 1, 2010 - March 31, 2012
Mentor:
Rudolph Tanzi, Ph.D.
Massachusetts General Hospital
|
Summary: In this study, we are exploring the idea that newly discovered Alzheimer’s disease associated mutations in the Alzheimer’s diseaseAM10 gene attenuate the function of ADAM10. This is being accomplished by generating and characterizing genetically modified mice over-expressing either wild-type or mutant forms of ADAM10. We are also assessing the effects of these mutations on Alzheimer’s disease-like characteristics in a mouse model of the disease.
More details
Program: Alzheimer's Disease
Award Type: Research Fellowship
$100,000
|
Hwan-Ching Tai, Ph.D.
Massachusetts General Hospital
Boston, MA
Title:
Proteasome-interacting proteins in tau degradation
Non-Technical Title:
Studying the Clearance of Proteins that Accumulate in Alzheimer's disease
Duration:
April 1, 2010 - March 31, 2012
Mentor:
Bradley Hyman, M.D., Ph.D.
Massachusetts General Hospital
|
Summary: Characteristic accumulations of the “Tau” protein is one of the most important hallmarks of Alzheimer's disease, and tau turnover is a major focus in the study of Alzheimer’s disease causes and treatment. This study seeks to understand the molecular mechanism of tau degradation by the “ubiquitin-proteasome” system, which is the most important proteolytic system in neurons, necessary for the destruction of damaged or unneeded proteins. The focus of this study is on proteasome-interacting proteins that may help deliver misfolded tau to the proteasome for digestion.
More details
Program: Alzheimer's Disease
Award Type: Research Fellowship
$100,000
|
Gopal Thinakaran, Ph.D.
University of Chicago
Chicago, IL
Title:
Microdomain Localization And Trafficking Of BACE1
Non-Technical Title:
Understanding The Mechanisms Of Alzheimer's Disease Amyloid Production
Duration:
April 1, 2009 - March 31, 2012
Co-Investigator(s):
Angele Parent, Ph.D.
University of Chicago
|
Summary: This proposal investigates BACE1, one of the enzymes critical for the production of Alzheimer's disease amyloid beta production. We are interested in deciphering the molecular principles of BACE1 trafficking in lipid rafts and non-raft domains using biochemical and live cell imaging approaches in order to elucidate the cell biology of BACE1 processing of amyloid precursor protein (APP). Our studies will uncover novel and significant basic insights into cellular processes that modulate amyloid beta production, thus contributing to the development of strategies aimed at reducing amyloid beta burden.
More details
Program: Alzheimer's Disease
Award Type: Standard
$400,000
|
|
Sheue-Houy Tyan, Ph.D.
University of California, San Diego
La Jolla, CA
Title:
Role of APP and Abeta-induced synaptic dysfunction
Non-Technical Title:
The cause of Alzheimer's disease
Duration:
April 1, 2010 - March 31, 2012
|
Summary: In this project, we are using the recently generated BRI-amyloid beta42 transgenic mouse line that offers the unique opportunity to examine amyloid beta-induced synaptic changes in the absence of APP over-expression. The study will provide insights into the potential causes of synaptic dysfunction in Alzheimer’s disease.
More details
Program: Alzheimer's Disease
Award Type: Pilot
$150,000
