Alzheimer’s disease (AD) occurs more frequently in diverse populations (ie: African Americans and Hispanics) than in white populations. This proposal seeks to investigate the role of a gene shown to be a risk factor for AD, ABCA7, and the consequence of a mutation that was first identified in African Americans. Stem cell lines have been generated from African Americans with this deletion and both neurons and cells involved in immunity, microglia, will be created. Using these two cell types, we will investigate how this deletion may affect the normal way neurons and microglia develop, and how that may lead to AD.
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- Holly Cukier, PhDUniversity of Miami, Miller School of Medicine (Coral Gables, FL)ID:A2018197SCo-principal Investigators:Derek Dykxnoorn, PhDJuly 1, 2018 to June 30, 2021Alzheimer's DiseaseStandard$300,000
- Xiangrun Huang, PhDUniversity of Miami, Miller School of Medicine (Miami, FL)
Glaucoma, a leading cause of blindness worldwide, damages a type of neuronal cells called retinal ganglion cells and their nerve fibers, known as axons, in the eye. Early detection of abnormities of the nerve fibers can permit early medical intervention to prevent vision loss in glaucomatous patients. The proposed research will develop a new optical imaging method that detects abnormities of the light reflected by the nerve fibers. The new approach can provide sensitive detection of the abnormities that occur at early stages of glaucoma. If successful, the developed methods can be readily translated to clinical use and provide clinicians with a new means to sensitively detect early glaucomatous damage, opening an early therapeutic window for the prevention of glaucomatous damage and vision loss.ID:G2018148July 1, 2018 to June 30, 2020GlaucomaStandard$150,000
The Dr. Douglas H. Johnson Award recipient
- Chao Wang, PhDWashington University School of Medicine (Saint Louis, MO)
Tau protein aggregation in neurons is one of the hallmarks of Alzheimer’s disease (AD). The APOE gene is a strong risk factor for AD and directly affects tau pathology and tau-mediated neurodegeneration. Therefore, we will ask if decreasing apoE levels in the brain can alter tau aggregation and tau-induced neurodegeneration, and we will also try to determine how apoE exerts its effects on tau. Understanding these questions will potentially help us to develop novel treatments for AD.ID:A2018128FJuly 1, 2018 to June 30, 2020Alzheimer's DiseasePostdoctoral Fellowship$150,000
- Joshua Grill, PhDUniversity of California, Irvine (Irvine, CA)
The single greatest barrier to advances in Alzheimer’s disease (AD) treatment is poor recruitment to clinical trials of promising therapies. Most of these clinical trials now enroll patients with mild cognitive impairment (MCI), which in many cases may be a “prodromal” form of AD that exists before full-blown dementia develops. This project will identify the challenges to enrolling these patients in clinical trials and identify methods to improve recruitment to these critical studies.ID:A2018405SJuly 1, 2018 to June 30, 2021Alzheimer's DiseaseStandard$300,000
- Celeste Karch, PhDWashington University School of Medicine (Saint Louis, MO)
Several lines of evidence suggest that inflammation and altered function of the cell types in the brain involved in inflammation, such as microglia, represent an early and critical driver of Alzheimer’s disease (AD). Our group has recently shown that a chemokine receptor type 4 (CXCR4) found in the cell types that mediate inflammation in the brain, such as microglia, contributes to tauopathies, such as progressive supranuclear palsy, frontotemporal dementia, corticobasal degeneration, and AD. The objective of this study is to begin to determine how CXCR4 drives AD. Together, the findings from this study will define the function of a new gene that increases risk for AD and other tauopathies and will shed light on its role in disease processes.ID:A2018349SJuly 1, 2018 to June 30, 2021Alzheimer's DiseaseStandard$300,000
- Joseph Castellano, PhDIcahn School of Medicine at Mount Sinai (New York, NY)
Possession of the APOE-ε4 gene confers a strong risk for earlier onset of Alzheimer’s disease (AD), a devastating brain disorder that damages brain synapses, or connections between neurons, and ultimately the neurons themselves that are responsible for memory and learning, as well as executive function. While it is clear that AD creates widespread damage within the brain itself, it is unclear whether the upstream cause of the disease may lie in changes that occur in the blood, ultimately influencing brain health. Support for this hypothesis can be found in the context of normal aging in which blood factors from old individuals drive characteristics of aging. This proposal will directly investigate how manipulating proteins in the blood influences the impact that the risk-conferring APOE-ε4 gene has on Alzheimer’s disease and the extent to which APOE- ε4’s harmful effects can be rescued with more neutral forms of the gene. The results possibly will provide fresh insights into new treatment avenues.ID:A2018213SJuly 1, 2018 to June 30, 2021Alzheimer's DiseaseStandard$300,000
- Mickael Audrain, PhDIcahn School of Medicine at Mount Sinai (New York, NY)
Neuroinflammation in the brain may be caused in part by neurodegenerative diseases such as tauopathies and Alzheimer’s disease. The brain’s resident immune cells, called microglia, are the resident “garbage disposal cells” of the brain and thereby play key roles in any inflammatory processes. Using a novel multiscale computational approach, a team from Mount Sinai identified the protein Tyrobp as a causal regulator controlling the garbage disposal actions of microglia. To understand the role of Tyrobp in tauopathies, we generated new genetically-manipulated tauopathy-model mice that are rendered deficient for Tyrobp. Characterization of these mice will help to determine how Tyrobp modifies inflammation and the progression of tauopathy, thereby greatly influencing this field of research.ID:A2018253FMentors:Sam Gandy, MD, PhDJuly 1, 2018 to June 30, 2020Alzheimer's DiseasePostdoctoral Fellowship$150,000
- Jessica Cooke Bailey, PhDCase Western Reserve University (Cleveland, OH)
We know that genetics and environment play a role in glaucoma risk, but most of the people who have been studied are different on many levels. We want to study glaucoma in the Amish, a group that is essentially a very large family. We think that by understanding glaucoma risk in the Amish, we can learn more about the genes and pathways that influence this disease. This knowledge will serve to better inform preventative and treatment strategies relevant to the millions of people throughout the world who will likely acquire glaucoma unless new ways of understanding disease risk and prevention are developed.ID:G2018042Co-principal Investigators:Jonathan L. Haines , PhDJuly 1, 2018 to June 30, 2020GlaucomaStandard$150,000
- Xi-Qin Ding, PhDUniversity of Oklahoma Health Sciences Center (Oklahoma City, OK)
Age-related macular degeneration (AMD) is characterized by a progressive death of retinal pigment epithelium (RPE) cells in the central macular region of the retina and subsequent degeneration of light-sensitive neurons (photoreceptors). Oxidative stress/damage to the RPE is recognized as the core pathogenic lesion of the disease. In this project, we study the role of thyroid hormone in RPE oxidative stress/damage and investigate whether suppression of thyroid hormone activity protects RPE against oxidative damage.ID:M2018107Collaborators:Goldis Malek, PhDJuly 1, 2018 to June 30, 2020Macular DegenerationStandard$160,000
Elizabeth Anderson Award recipient.
- Yingbin Fu, PhDBaylor College of Medicine (Houston, TX)
Age-related macular degeneration (AMD) is a disease that blurs the sharp, central vision you need for everyday activities, such as seeing faces, reading, sewing, and driving. Advanced AMD can be classified into the dry form (gradual breakdown of the light-sensitive cells in the macula) and the wet form (leaky blood vessels growing under the retina). The current treatment for wet AMD is suboptimal, while there is no treatment available for dry AMD. We propose to develop a novel and effective treatment for both the wet and dry forms of AMD by using a protein called AIBP (apolipoprotein A-I binding protein).ID:M2018142July 1, 2018 to June 30, 2020Macular DegenerationStandard$160,000
This grant is made possible by support from The Helen Juanita Reed Award for Macular Degeneration Research.