In neovascular age-related macular degeneration (AMD), the sprouting of new blood vessels (angiogenesis/neovascularization) leads to the death of the nerve cells of the retina. Neovascular AMD places a substantial burden on patients and the healthcare system. Current approaches to block new blood vessels from forming are not effective in many patients and they have serious side effects. There’s an urgent need for effective new ways to prevent these faulty new blood vessels from forming, but not affect the health of retinal nerve cells or the normal blood vessels. To address this need, we are developing a genetic animal model where we can rapidly identify novel, safe and effective drugs for the treatment of neovascular AMD.
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BrightFocus drives innovative research worldwide on Alzheimer’s, macular degeneration, and glaucoma.
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- Sarah McFarlane, PhDUniversity of Calgary (Canada)ID:M2017002July 1, 2017 to June 30, 2019Macular DegenerationStandard$123,160
- 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
- Derek Welsbie, MD, PhDUniversity of California, San Diego (La Jolla, CA)
Nerve cells called retinal ganglion cells (RGCs) form the connection between the eye and the brain. In glaucoma, these nerve cells die and vision is permanently lost. We have previously shown that a protein called dual leucine zipper kinase (DLK) is critical for the death of these cells. Thus, this proposal seeks to develop a gene therapy vector that might interfere with DLK and prevent RGC death and accompanying vision loss.ID:G2017212Collaborators:Donald J. Zack, MD, PhDJuly 1, 2017 to June 30, 2019GlaucomaStandard$150,000
Recipient of the Dr. Douglas H. Johnson Award
- Krishnakumar Kizhatil, PhDThe Jackson Laboratory (Bar Harbor, ME)
Glaucoma is a devastating neurodegenerative disease that causes blindness. Glaucoma results from increased pressure in the eye; however, the mechanistic basis of the pressure increase is largely undetermined. Neurons innervating the eye play a role in controlling pressure, but again the specific mechanisms are not clear. We will determine the mechanistic basis of neuronal control of eye pressure using mice and modern imaging and molecular methods.ID:G2017152Collaborators:Simon W. M. John, PhDJuly 1, 2017 to June 30, 2019GlaucomaStandard$150,000
- Linda Zangwill, PhDUniversity of California, San Diego
Numerous studies have suggested that vascular factors (blood supply) are involved in the development of glaucoma, but it is currently not known whether a reduction in blood supply to the eye is a cause or an effect of the glaucoma disease process. Recent advances in imaging technology have made it possible to visualize and measure the retinal blood supply, as well as assess the deep layers of the optic nerve head, including the lamina cribrosa, during routine eye exams. This prospective clinical research study will investigate whether changes in the retinal blood supply precede or follow other structural and mechanical changes in glaucoma.ID:G2017122Co-principal Investigators:Min Suh Hee, MDJuly 1, 2017 to June 30, 2019GlaucomaStandard$150,000
- Matthew Van Hook, PhDTruhlsen Eye Institute, University of Nebraska Medical Center (Omaha, NE)
Glaucoma is a disease often associated with increased intraocular pressure (IOP) that causes blindness when the nerve cells that carry information from the eye to the brain, called retinal ganglion cells (RGCs) die. One particular group of RGCs, called melanopsin RGCs, play a critical role in regulating sleep, mood, and pupil constriction, and it is likely that their function is altered during glaucoma. This project seeks to determine how melanopsin RGC performance and signaling to the brain are altered at early stages of glaucoma, after increases in eye pressure, but before RGCs die. This will help doctors understand some of the earliest signs of glaucoma and may lead to the development of entirely new ways to detect the disease at its earliest stages, and thus prevent blindness.ID:G2017027Collaborators:Shan Fan, MD; Deepta Ghate, MDJuly 1, 2017 to June 30, 2019GlaucomaStandard$150,000
- Yong Wang, PhDWashington University School of Medicine (St. Louis, MO)
Our new PET-MRI [positron emission tomography–magnetic resonance imaging] method takes pictures of the brain in elderly people. Whereas these PET-MRI images have commonly been used to identify tumors or strokes in patients, we have found a new way to use PET-MRI to measure the brain’s injury and immune response. We have found this imaging method to be very useful in patients with multiple sclerosis, and now we are able to use it in patients who have Alzheimer’s disease (AD), in order to get a sense of the problems that might be developing in their brain before memory problems occur. We hope that our new method also will be useful in clinical trials testing new drugs for early intervention with AD.ID:A2017330SCollaborators:Yi Su, PhD; Jinbin Xu, PhDJuly 1, 2017 to June 30, 2020Alzheimer'sStandard$300,000
- Daniel Saban, PhDDuke University Eye Center (Durham, NC)
The deterioration of light-sensing nerves of the retina contributes to vision loss in patients with age-related macular degeneration (AMD). The immune system is thought to contribute to this deterioration, but how this is accomplished remains elusive. Our grant project seeks to identify the specific immune cell type that contributes to vision loss and to devise a strategy that neutralizes such cells to ultimately help preserve vision in patients suffering from age-related macular degeneration.ID:M2017183July 1, 2017 to June 30, 2019Macular DegenerationStandard$160,000
- Fenquan Zhou, PhDJohns Hopkins University (Baltimore, MD)
The proposed study aims to investigate two novel approaches for promoting long distance (ie, eye to brain) optic nerve regeneration. First based on our completed genetic study we will test if pharmacological inhibition of an identified protein via direct eye injection can promote long distance optic nerve regeneration or whether, based on strong preliminary data, manipulation of another novel gene can induce such regeneration. The project will identify a potential translational approach for promoting optic nerve regeneration, and also open a new avenue for identifying novel gene targets that can be manipulated to enhance optic nerve regeneration.ID:G2017037July 1, 2017 to June 30, 2019GlaucomaStandard$150,000
This grant is made possible in part by a bequest from the Timothy Miles Charitable Trust.
- Chris Schaffer, PhDCornell University (Ithaca, NY)
Blood flow to the brain is reduced by about one-third in Alzheimer’s disease (AD) patients and this blood flow reduction contributes to the memory problems of the disease. In mice that get Alzheimer’s, we recently discovered that the blood flow reduction is due to white blood cells that get stuck and block blood flow in individual capillaries, which are the brain’s smallest vessels. When we eliminated these capillary stalls, the Alzheimer mice showed a 30 percent increase in brain blood flow as well as improved performance on memory tasks. Here we propose to screen drugs that interfere with white blood cell adhesion and that have already been proven to be safe in humans to find compounds that reduce capillary stalling and could be tried in AD patients.ID:A2017488SJuly 1, 2017 to June 30, 2020Alzheimer'sStandard$300,000