Vision loss in AMD is caused by the dysfunction and loss of the retinal pigment epithelium (RPE), a pigmented layer of cells which support the photosensitive photoreceptors. RPE health and protective functions depend on their metabolism, the highly regulated process controlling energy production and by-products detoxification. Here we will study a novel pathogenic mechanism responsible for impaired RPE metabolism and progression to the advanced neovascular form of AMD.
See what research we fund.
- Magali Saint-Geniez, PhDThe Schepens Eye Research Institute, Harvard Medical School (Boston, MA)ID:M2018064July 1, 2018 to June 30, 2020Macular DegenerationStandard$160,000
- 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
- Yuan Lei, PhDEye and ENT Hospital of Fudan University (Shanghai, China)
The most effective therapy for glaucoma is reducing eye pressure, but it is not understood how the pressure in the eye is regulated. MicroRNAs (miRNAs) are very small genetic sequences that can regulate the expression of many genes. In fact, a single miRNA is so powerful that it can modulate several genes. The aim of this project is to understand the role of a very important miRNA in regulating intraocular pressure (IOP). This may be a very effective new way to treat elevated eye pressure in glaucoma.ID:G2018112July 1, 2018 to June 30, 2020GlaucomaStandard$99,546
- Rouzbeh Amini, PhDThe University of Akron (Akron, OH)
The shape of the iris and how it deforms in response to light (ie, pupil dilation or constriction) are important factors in understanding the mechanism of glaucoma. Similar to any other tissue that deforms (eg, blood vessels or skeletal muscles), if the iris is stiffer, it deforms differently, which has been the case in some glaucoma patients. Unlike previous studies, in which surgically removed pieces of the iris were used for quantifying the stiffness, we aim to combine noninvasive imagining techniques currently used in eye clinics with a novel computer model to estimate iris stiffness. We also aim to understand how stiffening of the iris affects the shape of its comprising cells during the pupil’s responses to light, because we believe that cellular-level deformation is an important factor in the regulation of activities in those cells.ID:G2018177Co-principal Investigators:Syril K. Dorairaj, MDJuly 1, 2018 to June 30, 2020GlaucomaStandard$150,000
- Suchismita Acharya, PhDUniversity of North Texas Health Science Center at Fort Worth (Fort Worth, TX)
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.ID:G2018056July 1, 2018 to June 30, 2020GlaucomaStandard$150,000
- William Scott, PhDUniversity of Miami, Miller School of Medicine (Miami, FL)
Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in older adults in the United States. The factors that determine progression from early AMD (with little vision loss) to advanced AMD (with more severe vision loss) are poorly understood. We will use detailed clinical examinations of the eye and large-scale genetic analysis to identify new genetic factors that are associated with changes in the eye over time and with development of advanced AMD. The results of this study will improve our understanding of the AMD disease process and provide potential avenues for development of targeted therapies.ID:M2018112Co-principal Investigators:Margaret A. Pericak-Vance, PhDCollaborators:Jonathan L. Haines, PhD; Stephen G. Schwartz, MD; Jaclyn L. Kovach, MD; SriniVas Sadda, MDJuly 1, 2018 to June 30, 2020Macular DegenerationStandard$160,000
This grant is made possible by support from Dr. H. James and Carole Free.
- Jill M. Goldstein, PhDMassachusetts General Hospital and Harvard Medical School (Boston, MA)
This project will support the launching of a comprehensive effort (integrating clinical, physiological and brain biology traits) to identify in early midlife biomarkers for Alzheimer’s disease risk informed by sex differences in brain aging and memory decline. This is one of the first projects to comprehensively assess multiple predicted biomarkers for Alzheimer’s risk in middle age and relate them to brain scans, physiology, genetics, and clinical data with a specific focus on incorporating differences between men and women in Alzheimer’s development.ID:CA2018607March 30, 2018 to March 29, 2020Alzheimer's DiseaseStandard$1,112,000
- Ann-Charlotte Granholm-Bentley, PhD, DDSUniversity of Denver (Denver, Colorado)
The focus of this special project is to develop a strong collaborate network between six different research groups focused on providing much-needed information about the Down syndrome population, of which as many as 80 percent have Alzheimer’s pathology by the time they are in their 50s and 60s. Although there are many centers and researchers that focus on Alzheimer’s in the general population, few of them focus on people with Down syndrome. The information generated by our project will be of great help to those with Down syndrome and those with Alzheimer’s disease.ID:CA2018010Co-principal Investigators:Elizabeth Head, PhD; Elliott Mufson, PhDNovember 1, 2017 to October 31, 2022Alzheimer's DiseaseStandard$435,050
- Peter Tessier, PhDUniversity of Michigan (Ann Arbor, MI)
Alzheimer’s disease (AD) is linked to proteins that misbehave and stick together into protein particles that are toxic to brain cells. Early detection of this dreaded disease requires the generation of imaging molecules that can enter the brain and selectively tag the toxic protein particles in different parts of the brain. We aim to use an innovative design and evolution method for generating imaging probes specific for particles of one of the most harmful Alzheimer’s proteins (tau). We will use these novel probes to image toxic tau protein particles in the brains of mice used as models of AD, with the long-term goal of translating this technology to humans for early and accurate disease detection.ID:A2017395SSeptember 1, 2017 to August 31, 2020Alzheimer's DiseaseStandard$300,000
- Ephraim F. Trakhtenberg, PhDUniversity of Connecticut Health Center (Farmington, CT)
The biological molecular mechanisms controlling the growth of connections in the central nervous system (CNS) are still poorly understood. The inability of the eye to regenerate such connections to the brain is the key reason why vision is lost from optic nerve damage, which can happen in a disease such as glaucoma, cannot be restored. We propose to identify novel biological regulators of the intrinsic ability of the retinal cells to regrow such connections between the eye and the brain. These studies could lead to the development of therapeutics for restoring simple visual abilities to those who became blind due to angle-closure glaucoma, and possibly other types of glaucoma.ID:G2017204July 1, 2017 to June 30, 2019GlaucomaStandard$150,000