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BrightFocus Research Grants Funding
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Alzheimer's Disease Research - Current Awards

Dr. Katrin Andreasson

Katrin Andreasson, MD

Stanford University
Stanford, CA

Title: Inhibiting Tryptophan Metabolism in Alzheimer’s Disease
Non-Technical Title: Preventing and Treating Alzheimer’s Disease by Inhibiting Tryptophan Metabolism
Duration: July 1, 2014 - June 30, 2017

Summary: The proposed work will determine whether degradation of the amino acid tryptophan by the enzymes TDO2 and IDO1 plays a role in the development of Alzheimer’s disease (AD). We will use genetic and pharmacologic approaches in a mouse model of AD to identify mechanisms of action of these enzymes in early and late stages of AD development. Successful completion of these studies may lead to novel preventive and therapeutic strategies to delay onset of AD in at-risk aging populations.
More details

Program: Alzheimer's Disease
Award Type: Standard
$250,000



Dr. Steven E. Arnold

Steven E. Arnold, M.D.

University of Pennsylvania
Philadelphia, PA, United States

Title: Effect of Insulin Sensitizer Metformin on Alzheimer’s Disease Biomarkers
Non-Technical Title: A Trial of the Anti-Diabetes Drug Metformin for Alzheimer's Disease
Duration: July 1, 2012 - June 30, 2015

Summary: Previous studies and Dr. Steven Arnold’s laboratory work have shown that the brain in Alzheimer's disease is resistant to the healthy growth effects of insulin and that re-sensitizing brain cells to insulin may be a useful therapeutic strategy. Dr. Steven Arnold and colleagues have identified the anti-diabetes drug, metformin, as a safe medicine that enters the brain and re-sensitizes insulin receptors. This proposal seeks to conduct an efficient clinical trial with metformin in people with mild cognitive impairment and early dementia due to Alzheimer's disease to determine its effect on cognitive functioning and physiological and biochemical biomarkers of Alzheimer's disease.
More details

Program: Alzheimer's Disease
Award Type: Standard
$300,000



Hirohide Asai, MD, PhD

Hirohide Asai, M.D., Ph.D.

Boston University School of Medicine
Boston, MA

Title: The Cellular Mechanism of Tau Dissemination
Non-Technical Title: A Novel Cellular Mechanism to Understand Spreading of Tau Aggregation in Alzheimer's Disease Brain
Duration: July 1, 2013 - June 30, 2015

Mentor:
Tsuneya Ikezu, M.D., Ph.D.
Boston University School of Medicine

Summary: This proposal is designed to characterize the molecular mechanism of how tau protein is involved in forming the toxic neurofibrillary tangles in the affected brain regions of Alzheimer’s disease and frontotemporal dementia. Dr. Asai’s team will determine if this is mediated by transfer of aggregated tau protein from nerve cell-to-nerve cell or from nerve cell-to-glia (non-neuronal brain cells). In addition, there will be specific focus on the role of microglia, the brain resident immune cells (called phagocytes), in the transport of tau across different brain regions in the diseased brain. This study is critically relevant to understand the progression of these devastating diseases with the goal to discover a potential therapeutic target.
More details

Program: Alzheimer's Disease
Award Type: Research Fellowship
$100,000



Dr. Michal Beeri

Michal Schnaider Beeri, PhD

Sheba Medical Center and Interdisciplinary Center (Israel)
The Icahn School of Medicine at Mount Sinai (New York, NY)

Title: Vascular Function and Cognition in Type 2 Diabetes
Non-Technical Title: Blood Vessel Function in Cognitive Impairment with Diabetes
Duration: July 1, 2014 - June 30, 2017

Co-PI(s):
David Tanne, MD
Sheba Medical Center

Summary: The risk for cognitive impairment and Alzheimer’s disease is increased in patients with Type 2 diabetes (T2D), possibly due to impairments in the structure and function of blood vessels in the brain. Previous studies have shown that problems in blood vessel functioning, which are reversible, occur prior to structural problems, and that treatment for impaired blood vessel functioning may prevent irreversible damage to their structure. We propose to study the role of blood vessel functioning and cognitive impairment in T2D patients to determine how different factors within T2D (for example blood glucose levels) affect this relationship. The results of this study may lead to treatments for the prevention of cognitive impairment in T2D and also may help us better understand preventable factors that weaken cognition in elderly people.
More details

Program: Alzheimer's Disease
Award Type: Standard
$250,000



Dr. Narayan Bhat

Narayan Bhat, Ph.D.

Medical University of South Carolina
Charleston, SC, United States

Title: Role of a Stress Kinase in AD Pathogenesis
Non-Technical Title: Defining the Role of a Signaling Pathway in Alzheimer's Disease
Duration: July 1, 2011 - June 30, 2015

Summary: The project investigates the role of a key cell signaling pathway commonly involved in cell stress and inflammatory responses i.e., p38 MAP kinase in multiple pathogenic processes of Alzheimer's disease (AD) including neuroinflammation, tau phosphorylation, amyloid deposition and synaptic dysfunction. The approach uses a genetic conditional knockout strategy to cell-specifically delete the kinase in microglia and forebrain neurons in a mouse model of AD. The outcome will provide mechanistic insight into AD-associated pathogenic processes and define the signaling pathway as a versatile treatment target for AD.
More details

Program: Alzheimer's Disease
Award Type: Standard
$399,873



Dr. David Brody

David Brody, MD, PhD

Washington University School of Medicine
St. Louis, MO

Title: Purification and Characterization of Amyloid-beta Oligomers from Human Brain
Non-Technical Title: Purifying the Most Toxic Forms of Beta Amyloid from the Brains of Patients with Alzheimer’s Disease
Duration: July 1, 2014 - June 30, 2017

Co-PI(s):
Michael Gross, PhD
Washington University

Summary: Alzheimer’s disease is the most common cause of problems with memory, thinking, and behavior in older people; it is most likely caused by accumulation of a small protein called beta amyloid. Despite decades of work, there is no cure or effective treatment for Alzheimer’s disease, in part because our attempts so far have not focused on the most toxic forms of beta amyloid. We have developed methods to accurately measure these toxic forms of beta amyloid in the brains of Alzheimer’s patients, and we now propose to purify these beta amyloid samples so that we can study them in detail. This project is vital because understanding the toxic forms of beta amyloid will help us efficiently design effective treatments to prevent them from forming, block their toxicity, or eliminate them from the brain.
More details

Program: Alzheimer's Disease
Award Type: Standard
$250,000



Dr. Virginie Buggia-Prevot

Virginie Buggia-Prevot, PhD

University of Chicago
Chicago, IL

Title: Role of EHD Proteins in Alzheimer's Disease Pathogenesis
Non-Technical Title: Understanding the Role of Novel Endocytic Proteins in Alzheimer's Disease Pathogenesis
Duration: July 1, 2014 - June 30, 2016

Mentor:
Gopal Thinakaran, PhD
University of Chicago

Summary: The goal of my research is to better understand the causes of Alzheimer’s disease by studying the mechanisms that contribute to the underlying pathology of the disease, in order to identify potential therapeutic targets. In the brain of individuals with Alzheimer’s disease, a toxic peptide called amyloid is overproduced and leads to dysfunction of memory functions and ultimately the death of the nerve cells. I recently found two proteins in a family called EHD (eps15 homology domain-containing proteins), which are involved in amyloid peptide production in cultured neurons. Our investigation will determine if there is an alteration of EHD in human brains that could facilitate amyloid overproduction, and will test whether amyloid overproduction could be blocked by abolishing the expression of EHD in mice that are engineered to develop Alzheimer’s disease pathology. Thus, our proposal is aimed at investigating neuronal mechanisms that are intimately associated with Alzheimer's disease with the goal of establishing EHD proteins as one of the molecular players in disease pathogenesis.
More details

Program: Alzheimer's Disease
Award Type: Research Fellowship
$120,000

Acknowledgements: This grant is made possible by a bequest from the Herbert Howlett Trust, in his memory.



Dr. Paramita Chakrabarty

Paramita  Chakrabarty, Ph.D.

University of Florida
Gainesville, FL

Title: Innate Immune System and Tauopathy
Non-Technical Title: How Inflammation in the Brain and Periphery Affects Brain Pathology in Common Dementias such as Alzheimer's Disease
Duration: July 1, 2013 - June 30, 2016

Co-PI(s):
Naruhiko Sahara, Ph.D.
University of Florida

Summary: One of the most important factors that underlie degeneration of neurons in an Alzheimer's disease patient brain is massive inflammation. Inflammation is a natural reaction of the body to toxins, bacteria, and foreign particles. Cytokines are the messengers during inflammation and carry information between different cells. In the first part of the grant, using novel molecular biology techniques, the team of Drs. Chakrabarty and Sahara will try to understand whether the levels of cytokines and other related proteins are altered during the progressive development of abnormal brain changes in Alzheimer’s disease mouse models. Further, using different classes of cytokines in the brains of these mice, the team will explore whether one class of cytokines ('inflammatory') drive the disease and kill neurons in the process, whereas the opposing kind ('anti-inflammatory' cytokines) improves the disease and are protective.
More details

Program: Alzheimer's Disease
Award Type: Standard
$249,840

Acknowledgements: This grant is made possible in part by a bequest from the Helen Veronica Coyne Trust.



Dr. Jasmeer Chhatwal

Jasmeer P. Chhatwal, M.D., Ph.D.

Massachusetts General Hospital, Harvard Medical School
Boston, MA, United States

Title: Cross-Sectional and Longitudinal Network Degradation in Genetic and Sporadic AD
Non-Technical Title: Decay of Memory Networks in Alzheimer’s Disease
Duration: July 1, 2013 - June 30, 2015

Mentor:
Reisa Sperling, M.D., M.M.Sc.
Massachusetts General Hospital / Brigham and Women’s Hospital / Harvard Medical School

Summary: The goal of this study is to better differentiate normal aging and early Alzheimer’s disease (AD) by using MRI and PET imaging to examine the health of neural networks that allow us to store and retrieve memories. In addition to providing us with a better fundamental understanding of how neurodegenerative diseases like AD affect the brain, these studies will refine the use of imaging techniques in clinical trials and thereby improve drug development in AD.

Dr. Chhatwal and his research colleagues are very fortunate to have access to a large amount of imaging data from young individuals with genetic mutations that inevitably lead to early-onset dementia (often at age 40-50) who are participating in the Dominantly Inherited Alzheimer Network (DIAN) study, an international consortium led by investigators at Washington University in St. Louis. These data will be compared with imaging data from a wide variety of individuals, including cognitively normal young and older adults, as well as older individuals with Mild Cognitive Impairment and Alzheimer’s disease. With these unique and diverse datasets, and using novel analytic tools that were developed by Dr. Chhatwal and his colleagues, they can ask questions about how aging affects the brain and whether these changes are fundamentally different from those seen in AD.

This study makes use of four main types of imaging: (1) Functional connectivity MRI, to determine which parts of the brain are working together in networks; (2) Structural MRI, to very accurately measure the size of each fold and region of the brain; (3) Amyloid PET, to measure how much amyloid (the protein that clumps together to form plaques in brains of patients with AD) is in the brain; and (4) FDG PET, to see how much glucose (sugar) is used in each part of the brain. Together with information about memory performance by each of the subjects, these types of images provide a uniquely detailed picture of the brain’s health in normal and impaired subjects. By combining the information from these different types of imaging, Dr. Chhatwal and his colleagues will identify patterns of brain changes that indicate the earliest stages of AD, and use this information to determine the efficacy of experimental medications in Alzheimer’s prevention trials.

Dr. Chhatwal is very grateful for the participation of the many research subject volunteers, and for the support of those willing to provide funding for these exciting studies.
More details

Program: Alzheimer's Disease
Award Type: Research Fellowship
$100,000



Dr. Se Hoon Choi

Se Hoon Choi, Ph.D.

Massachusetts General Hospital
Boston, MA

Title: ADAM10 Regulates Adult Hippocampal Neurogenesis
Non-Technical Title: Investigating Whether ADAM10 Protein Modulates Birth of New Neurons in Adult Brain
Duration: July 1, 2013 - June 30, 2015

Mentor:
Rudolph E. Tanzi, Ph.D.
Massachusetts General Hospital

Summary: Alzheimer’s disease (AD) destroys brain cells, causing memory loss and problems with thinking and behavior severe enough to affect work, lifelong hobbies, and social life. New neurons are born in the adult brain (called “adult neurogenesis") and this process is impaired in AD, suggesting that impaired cognitive function in AD might, at least, in part, be due to impaired neurogenesis in the adult brain. ADAM10 is a protein that plays an important role in AD, as it prevents the generation of a toxic protein that causes AD. Dr. Choi’s team hypothesizes that ADAM10 also plays critical roles in adult neurogenesis, and they propose various animal and cell culture experiments to validate their hypothesis.
More details

Program: Alzheimer's Disease
Award Type: Research Fellowship
$100,000



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Last Review: 08/30/13