Glaucoma is a blinding disease and it is estimated that over 76 million people will be affected by this disease by 2020. It is associated with elevated eye pressure and progressive death of retinal ganglion cells (RGCs), as well as degeneration of the optic nerve head (which connects the brain to the eye). Nitric oxide (NO), a small gaseous molecule, is known to act as antioxidant, and is a key player in relaxing the smooth muscle cells and protecting damaged blood vessels. NO has the potential to reduce eye pressure, with high possibility of protecting the neural cells; however, free radicals generated during optic neuropathy may deplete nitric oxide bioavailability. Our group is working on discovering multi-functional small molecules that may be used for glaucoma treatment to decrease eye pressure and protect neurons, retinal ganglion cells from death.
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- Suchismita Acharya, PhDUniversity of North Texas Health Science Center at Fort Worth (Fort Worth, TX)ID:G2018056July 1, 2018 to June 30, 2020GlaucomaStandard$150,000
- Farid Rajabli, PhDUniversity of Miami, Miller School of Medicine (Coral Gables, FL)
The strongest risk gene identified for Alzheimer disease (AD) is APOE. However, this gene does not increase the risk for AD in every ethnic population. For example, individuals with an African ethnic background do not seem to be very affected by this variation. This is due to the fact that individuals from different races/ethnicities harbor genetic differences at the site of the APOE gene. This is why it is important to study populations separately and to take into account their genetic background, also called local ancestry, when analyzing the genetic effect on the disease. We propose to explore the relationship between local ancestry of African-American and Caribbean-Hispanic people and AD risk genes. We will facilitate the discovery of ethnic-specific genes and genetic changes increasing the risk for AD. This approach will allow us to move a further step toward personalized and precision medicine.
ID:A2018556FMentors:Margaret A. Pericak-Vance, PhD; Gary W. Beecham Jr., PhDJuly 1, 2018 to June 30, 2020Alzheimer's DiseasePostdoctoral Fellowship$150,000
- 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.
- Rosario Fernandez-Godino, PhDMassachusetts Eye and Ear Infirmary, Harvard Medical School (Boston, MA)
Age-related macular degeneration (AMD) affects more than 2 million individuals in the US and it will reach 3 million by 2020. Current therapies can improve vision only in some patients with advanced AMD; unfortunately, there is no effective therapy that prevents disease progression in patients with early disease or genetic predisposition. My aim is to create a cell-based model to discover the primary mechanisms activated by the combination of aging and genetic variants in complement genes in patients with early AMD; so that drugs can be designed to stop these mechanisms before they lead to major damage and legal blindness.ID:M2018115July 1, 2018 to June 30, 2020Macular DegenerationStandard$160,000
This grant is made possible by the Ivan Bowen Family Foundation.
- Timothy Miller, MD, PhDWashington University School of Medicine (St. Louis, MO)
Understanding the genetic risk factors associated with Alzheimer’s disease (AD) is important for identifying and directing successful treatment strategies. Of these risks, a gene known as the triggering receptor expressed on myeloid cells 2 gene, or TREM2, appears to increase the risk for developing AD by altering inflammatory responses and mediating the accumulation of toxic amyloid-beta protein in the brains of experimental mouse models. We propose a strategy that can reduce TREM2 expression in the context of AD and will investigate pathology and inflammation in response to TREM2 loss. Our results will identify the role of TREM2 in AD and help direct future TREM2-targeted therapies for AD patients.ID:A2018169SCollaborators:Ionis PharmaceuticalsJuly 1, 2018 to June 30, 2021Alzheimer's DiseaseStandard$298,335
- 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
- Jason Hassenstab, PhDWashington University (Saint Louis, MO)
We rely on complex memory and thinking skills to function in everyday life, however, these skills fluctuate constantly due to fatigue, stress, and anxiety—and these fluctuations increase as we age. Despite this, when we study people at risk for Alzheimer's disease (AD), we test memory and thinking in "one-shot" in an unfamiliar place (usually a clinic or hospital exam room). Some perform really well on a “good” day and others may perform more poorly on a “bad” day. These fluctuations make it extraordinarily difficult to measure true abilities. In this study, we propose to use smartphones to test memory and thinking in short "bursts" requiring less than 3 minutes each to complete. Participants can take tests wherever it is safe to use a smartphone and they take the tests multiple times per day, which provides much more accurate and reliable tests to better understand how memory and thinking change in very early AD.ID:A2018202SJuly 1, 2018 to June 30, 2021Alzheimer's DiseaseStandard$295,569
- Robert W. Nickells, PhDUniversity of Wisconsin-Madison (Madison, WI)
In order for cells to function normally, they need to make connections with other cells and with their environment. Breaking these connections will cause death. We believe that retinal ganglion cells (RGCs) lose these connections after optic nerve damage and that this may be one of the important initiators of their death in glaucoma. Understanding the importance of the link between ganglion cell connections and ganglion cell death may help us develop ways to prevent this pathology in optic neuropathies like glaucoma.ID:G2018166July 1, 2018 to June 30, 2020GlaucomaStandard$150,000
Recipient of the Thomas R. Lee Award for Glaucoma Research.
- Ottavio Arancio, MD, PhDColumbia University (New York, NY)
The cognitive and behavioral symptoms that characterize Alzheimer’s disease (AD) are thought to result from impaired communication between neurons in the brain at connections called synapses. Toxic forms of a protein called tau play a central role in AD and other neurodegenerative conditions, and recent data show that tau can interfere with synapses in multiple ways. These observations greatly underscore efforts to treat AD by blocking the pathological actions of tau. The goal of this project is to better understand how tau interferes with synaptic function so that we can develop effective strategies to block the impairments it causes.ID:A2018816SCo-principal Investigators:Russell Nicholls, PhDJuly 1, 2018 to June 30, 2021Alzheimer's DiseaseStandard$300,000
- Alex Smith, PhDUniversity of California, San Francisco (San Francisco, CA)
The healthy brain consumes large amounts of energy, ten times as much as other similarly sized regions of the body, but in Alzheimer’s disease (AD), the supply of energy-rich sugar from the blood to brain is reduced; it is not known why this happens. Blood vessels in the brain are surrounded by cells that contain a very large amount of a protein called aquaporin-4 that we think is involved in regulating how tightly these cells surround the vessels. In AD the amount of aquaporin-4 around vessels is reduced and we believe this causes the cells to swell around the vessels, blocking sugar from getting into the brain. We propose to do experiments that will test this idea and consider new therapies to remove the block for sugar transport into the brain.ID:A2018351SJuly 1, 2018 to June 30, 2021Alzheimer's DiseaseStandard$300,000