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RESEARCH GRANTS2019-2024

The Glaucoma Foundaon is dedicated to improving the lives of people with glaucoma. The Foundaon works to encourage and support basic and applied research in glaucoma with a goal of preserving and restoring vision. The Foundaon oers grants to researchers striving to improve the lives of glaucoma paents through novel innovaons and scienc advances. Beginning in 2024, one-year grants of up to $75,000 will be made in the areas of Exfoliaon Syndrome and Exfoliaon Glaucoma, Pressure Independent Mechanisms of Glaucoma, Neuroprotecon, and the Genecs of Glaucomas that aect people under the age of 40. Preference will be given to transformaonal research projects with high clinical signicance.

2019 RESEARCH GRANTSUnraveling the Proteolyc Landscape Regulang LOXL1 Implicaons in the Development of Pseudoexfoliaon Syndrome Principal Invesgator: Fernando Rodriguez Pascual, PhDCentro de Biologia Molecular “Severo Ochoa” (CSIC/UAM)Madrid, SpainWhile precise pathogenesis of PEX syndrome remains unknown, the idencaon of genec variants in the LOXL1 gene strongly associated to the disease has opened new avenues for the invesgaon on its molecular causes. The protein product of the LOXL1 gene belongs to the lysyl oxidase (LOX) family, a group of enzymes contribung to build the extracellular matrix (ECM) by promong the covalent associaon (cross- linking) of elasn and collagens. In parcular, LOXL1 plays an important role in the formaon of elasc bers, the ECM scaold mostly imparng elascity to animal ssues, an observaon very consistent with its idencaon as an integral part of the PEX deposits.With the support of a previous grant from TGF, we iniated a line of research aiming to invesgate the proteolyc processing of LOXL1 and its potenal implicaons in the development of PEX syndrome. Far from being completed, our results provide a glimpse of the complexity of the proteolyc landscape regulang LOXL1 expression and acvity, ancipang excing ndings potenally important for the development of PEX syndrome. Here we apply for a renewal of the support from TGF to accomplish the characterizaon of LOXL1 proteolyc regulaon and to invesgate its pathological relevance in the development of PEX syndrome.

2019 RESEARCH GRANTSGrowth Dierenaon Factor 15 Levels in Pseudoexfoliaon Glaucoma Principal Invesgator: Rajendra Apte, MD, PhDWashington University, St. Louis, MOThere are several kinds of glaucoma, all of which can lead to the death of cells in the eye that send visual informaon to the brain. Prevenng these cells from dying is an important part of the treatment for glaucoma. However, it can be dicult for physicians to idenfy which paents are at highest risk of developing glaucoma, or having their glaucoma get worse over me.Finding a marker, such as a protein in the eye whose presence might predict whether glaucoma will get worse, would make it possible for physicians to beer determine whether a paent should have surgery or another treatment. This project will study a protein called ‘growth dierenaon factor 15’ (GDF-15), which is associated with renal stress in rodents and humans. By measuring the levels of this protein in human paents with glaucoma before and aer surgery, we hope to understand whether there is a relaonship between GDF-15 levels in the eye, the severity of glaucoma, and success of glaucoma surgery. If high GDF-15 levels are linked with more severe glaucoma, it could be used as a marker to help determine treatment for paents at the highest risk of developing severe glaucoma.“With support from TGF, we are investigating whether a protein called Growth Dierentiation Factor-15 is a molecular biomarker for pseudoexfoliation (PXG). ese human pilot studies in patients with PXG can only be executed because of this generous grant support. We are analyzing the data and hope to publish our ndings before the end of the year.”

Metabolomic Analyses of Aqueous Humor of Pseudoexfoliaon GlaucomaPrincipal Invesgator: Sanjoy K. Bhaacharya, M. Tech, PhDBascom Palmer Eye InstuteUniversity of Miami Miller School of Medicine, Miami, FLWe will idenfy the small molecules in the clear uid of the front part of the eye termed aqueous humor. These small molecules are involved in all day-to-day funcons of biological ssues in the eye. This analysis will show a dierence in small molecules between pseudoexfoliaon glaucoma and normal eyes. Their addion (for example the molecules that provide energy) or removal (for example known toxic molecules) may be early intervenon strategies for treang pseudoexfoliaon glaucoma.2019 RESEARCH GRANTS“is grant has supported our critical experiments of metabolite proling and machine learning, and opened up the prospect for an extramural federal grant to fully investigate the initial mechanisms leading to deposit formation.”

New Understanding from Mouse Lines with Features of Pseudoexfoliaon SyndromePrincipal Invesgator: Yong Yuan, PhDCollege of Medicine, University of Cincinna, Cincinna, OhioPseudoexfoliaon syndrome is the most idenable cause of open-angle glaucoma. Animal models are crical tools for nding the cause of the disease and for tesng potenal treatment regimens. Currently, no animal model is available that can recapitulate the symptoms of this disease. We found features of pseudoexfoliaon syndrome in several mouse lines with genec defects aecng cellular funcons. The objecve of this proposal is to nd what is the common cause of the disease among these mouse lines. New knowledge obtained from this study will lead to a beer understanding of the disease as well as new strategies for combang the disease.2019 RESEARCH GRANTS“As a new investigator to the glaucoma eld, I am blessed to have the trust and the support from e Glaucoma Foundation in the form of grant awards and intellectual support at the ink Tank meetings. e grant helped me to collect critical data for a competitive NIH grant.”

Abnormal Extracellular Matrix Homeostasis of Trabecular Meshwork Cells in Pseudoexfoliaon Syndrome and Glaucoma Principal Invesgator: Katy Liu, MD, PhDDuke OphthalmologyDuke University School of MedicinePseudoexfoliaon glaucoma is the most common glaucoma with an idenable cause. However, there is no targeted treatment for pseudoexfoliaon glaucoma. The trabecular meshwork lies within the drain of the eye, and it has the highest resistance to oulow of eye uid or aqueous humor. Many sciensts theorize that the trabecular meshwork cells put down dysfunconal surrounding matrix, or extracellular matrix, which provides support for the cells. There is no suitable model to study the extracellular matrix of trabecular meshwork cells. For the rst me, we have grown trabecular meshwork cells from pseudoexfoliaon donors. This powerful tool will allow us to determine alteraons the trabecular meshwork extracellular matrix, and we have preliminary data to support this idea. We will also determine the eect of extracellular matrix on the biomechanical properes of trabecular meshwork cells, or the cell’s rigidity, which directly aects resistance to oulow of aqueous humor. This study is crical to further our understanding the role of the extracellular matrix in the mechanism of pseudoexfoliaon disease. With this knowledge, the extracellular matrix could be targeted by future drug and medical therapies. 2019 RESEARCH GRANTS

2019 RESEARCH GRANTSRole of LOXL1 Acvity in TGF-Beta 1-Mediated Fibrosis in the Convenonal Oulow PathwayPrincipal Invesgator: Heather Schmi, BS, MS, PhD Duke University, Durham, NC The proposed research is designed to invesgate the regulatory role of the LOXL1 protein that is associated with risk of pseudoexfoliaon glaucoma. We are interested in how LOXL1 acvity contributes to elevaon in eye pressure that is typical of pseudoexfoliaon glaucoma. Specically, we will invesgate the relaonship between LOXL1, a signaling molecule called TGF-beta 1 (Transforming Growth Factor) and eye pressure, using a mouse model. TGF-beta 1 is oen elevated in eyes of people with pseudoexfoliaon glaucoma, and it is known to induce “scarring” that causes elevated eye pressure. Results from this project will provide a beer understanding of disease mechanism and may lead to targeted clinical intervenons for pseudoexfoliaon glaucoma.“is grant has provided critical funding for technician salaries, biological materials, and animal care to complete these experiments. We believe that the results of this study will give us new insight into the role of LOXL1 in TGF-beta 1-mediated brosis in pseudoexfoliation glaucoma, potentially qualifying LOXL1 as a suitable drug target for pseudoexfoliation glaucoma treatment.”

2020 RESEARCH GRANTSIdenfying Glaucoma Risk Alleles in the LOXL1 Promoter Using a Massive Parallel Promoter AssayPrincipal Invesgator: John H. Fingert, PhDUniversity or IowaExfoliaon syndrome is a disease that causes accumulaon of brillar material (exfoliaon material) in ssues throughout the body, including the eye. Paents with exfoliaon syndrome are at high risk for glaucoma and vision loss, thus exfoliaon syndrome is a public health problem. The specic causes of exfoliaon syndrome are unknown, but hereditary is important. The genec basis of exfoliaon syndrome is complex and involves the interacon of many genec and environmental factors. Seven genec risk factors have been discovered, and one of these genes, LOXL1, is a potent risk factor for disease. In this applicaon, we propose experiments to determine the mechanism by which the LOXL1 gene confers risk for exfoliaon syndrome. Our hypothesis is that dozens of dierent genec mutaons together cause an abnormal amount of LOXL1 protein to be produced in the eye, which in turn damages the drainage structures of the eye and leads to glaucoma. With our proposal we will idenfy dozens of mutaons that alter LOXL1 producon in the eye using a DNA sequencing technique known as BiT-STARR-seq. The overall goal of these experiments will be to idenfy the specic cause of exfoliaon syndrome at the molecular level (i.e. LOXL1 gene mutaons).

THE BARRY FRIEDBERG AND CHARLOTTE MOSS GRANT AWARDAn-Fibroc Potenal of All-Trans Renoic Acid in Pseudoexfoliaon Syndrome and GlaucomaPrincipal Invesgator: Ursula Schlötzer-Schrehardt, PhDUniversity of Erlangen-NürnbergThe causes underlying the development of pseudoexfoliaon syndrome and its associated glaucoma, which is the most common type of secondary open angle glaucoma associated with a high risk of blindness, are not fully understood, and there is no specic treatment. This project addresses the current need for a beer understanding of the mechanisms of PEX pathogenesis and idencaon of therapeuc targets. It proposes to test the hypothesis that impaired renoic acid signaling is causally involved in the abnormal broc matrix process. It is further suggested that compounds smulang renoic acid signaling have a potenal to reverse the adverse broc eects of disease. It is ancipated that the ndings will idenfy novel pathomechanisms involved in the development of PEX glaucoma and advance the development of novel therapeuc approaches for the treatment of pseudoexfoliaon syndrome and glaucoma. Dr. Schlötzer-Schrehardt is a member of TGF’s Scienc Advisory Board. She is a professor at the University of Erlangen - Nürnberg’s Department of Ophthalmology where she has been cited as the world’s leading expert on the pathogenec mechanisms causing PEX and lauded for her tremendous contribuons to our knowledge of the cellular and molecular mechanisms that cause this disease.

Role of IGFBPL1 on Renal Ganglion Cell Survival in an IOP-independent Injury ModelPrincipal Invesgator: Kin-Sang Cho, PhDSchepens Eye Research InstuteGlaucoma is a globally unmet medical challenge because of its prevalence, devastang consequences and lack of eecve treatment. The disease leads to progressive loss of renal ganglion cells and vision. Our recent study idened a protein called insulin-like growth factor binding protein like-1 (IGFBPL1) that is a novel regulator of renal ganglion cells survival and nerve growth. Progressive loss of renal ganglion cells and their axons in the opc nerve is a characterisc feature of glaucoma, leading to vision loss. We recently observed lack of IGFBPL1 in mice exhibits progressive degeneraon of renal ganglion cells, which mimics the pathogenesis of IOP-independent glaucoma. It suggests that IGFBPL1 is a key player to maintain RGC survival in the adult. The proposed study will invesgate the regulatory networks of IGFBPL1 and the long-term eect of IGFBPL1 on the survival in a IOP-independent glaucoma model. Aer compleon of the proposed studies, we ancipate uncovering novel molecular targets for glaucoma therapy.2020 RESEARCH GRANTS

Renal Organoids to Study Disease Progression and Intervenon in GlaucomaPrincipal Invesgator: Miriam Kolko, MD, PhDUniversity of CopenhagenGlaucoma is characterized by the progressive loss of the renal ganglion cells (RGCs), and while IOP clearly plays a role, several lines of research have indicated that dysfuncon of the Müller glia (MG) play a key role in the pathophysiology.We hypothesize that vulnerability to RGC loss depends on MG􀂶s ability to protect theRGCs and that MG dysfuncon due to glaucoma will aect the essenal partnership between RGCs and the MG. We will look at two paents’ groups, denoted normal tension glaucoma (NTG) and ocular hypertension (OHT). In NTG paents, IOP is within the normal range, but paents sll experience glaucomatous RGC loss. We assume that NTG paents may have a specic MG dysfuncon leading to RGC loss. In contrast to NTG paents, paents with OHT have increased IOP but no evidence of glaucomatous damage. These paents may have a resistance due to a sustained healthy MG and are therefore able to withstand the high IOP. Unlike NTG paents, paents with OHT have increased IOP but no evidence of glaucomatous injury. They may have a resistance due to connued healthy MG and therefore are able to withstand the high IOP. Our hypothesis is that we can detect new neuroprotecve targets from MG derived from OHT paents as well as further idenfy both toxic and neuroprotecve targets in RGCs that have been exposed to MG from NTG or OHT paents, respecvely.2020 RESEARCH GRANTS

Schlemm’s Canal Catheterizaon a n d S u b s t a n c e D e l i v e r y i n L i v e M o n k e y sPrincipal Invesgator: Paul L. Kaufman, MDUniversity of Wisconsin MadisonGlaucoma is the leading cause of irreversible blindness. Its prevalence increases with age. Lowering pressure inside the eye is crical to glaucoma therapy, and slows progression of opc nerve damage and visual loss. Self- administered eye drops ulize various drugs that enhance uid oulow from or decrease uid formaon by the eye, reducing eye pressure. Most paents will require several classes of drop therapy, each self-administered one to three mes daily. Unfortunately, paent adherence to self-administered drop regimens is poor, because of age-related inrmies and the complexity of medical regimens for co-exisng condions. In live monkeys, we will inject viruses carrying genes that enhance uid oulow into the small drainage channel (Schlemm’s canal) that encircles the front part of the eye, permanently reducing the ow resistance of the major oulow pathway, reducing the viral load, avoiding o-target local and systemic adverse side eects, assuring consistent therapeuc ecacy, and relieving the paent’s physical and psychological burden We have designed and fabricated the ny catheters, mastered the microscopic injecon technique, constructed virus-gene vectors that work in cells and in organ-cultured monkey eyes, and are ready to move into live monkeys (this project) and then hopefully into human clinical trials.2021 RESEARCH GRANTS

DNA Methylaon and RGC Degeneraon in GlaucomaPrincipal Invesgator: Shahid Husain, PhDUniversity of South CarolinaGlaucoma is the second leading cause of blindness worldwide. Nearly 80 million people worldwide are believed to have glaucoma, including an esmated 3 million in the USA. Approximately 120,000 people are blinded by glaucoma accounng for 9-12% of all cases of blindness. Vision loss is caused by damage to the opc nerve, which connects eye to the brain for image formaon and recognion. In most cases of glaucoma, vision loss is coincident with elevated eye pressure. This pressure imbalance in the eye over a long period of me causes degeneraon of eye neuron, which ulmately leads to the blindness. During the progression of glaucoma, numerous factors including epigenecs play crucial role. Chemical reacons with the help of enzymes can modify DNA. Once DNA is chemically modied it will become ghtly packed and reduces it acvity for the producon of certain benecial factors such as neurotrophins. Neurotrophins are essenal components for the neuron of healthy eye. When DNA is ghtly packed it will not allow machinery to produces neurotrophins, as a result neurons will be deprived of neurotrophins and start to degenerate. Once sucient number of neurons are degenerated, it will lead to the blindness, as seen in glaucoma.LINDA AND KENNETH MORTENSON GRANT AWARD

Mouse Strain Specic Dierences in Intracranial Pressure and Suscepbility to GlaucomaPrincipal Invesgator: Colleen M. McDowell, PhDUniversity of Wisconsin MadisonGlaucoma is a silent, underdiagnosed, costly and debilitang disease and the only treatment opons for the disease include reducing elevated pressure within the eye. However, paents are somemes resistant to current established treatments and it is crucial to idenfy therapies and develop new treatments for glaucoma that can directly save the visual neurons from dying. We will ulize mouse models to study changes in pressure occurring on the eye neurons from both inside the eye and from the brain side of the eye in glaucoma to idenfy new protecon therapies.2021 RESEARCH GRANTS

2021 RESEARCH GRANTSTargeng Neuronal NAD Producon Through NMNAT2 Acvity for Neuroprotecon in GlaucomaPrincipal Invesgator: Pete A. Williams, PhD St Erik Eye HospitalOur research program has idened metabolic dysfuncon in the rena and opc nerve in experimental glaucoma animals and human glaucoma paents. We have discovered that an important molecule, ‘NAD’, declines in the rena and opc nerve during glaucoma, and increasing NAD levels using niconamide (a form of vitamin B3 and a precursor to NAD) prevents glaucoma in animals. Niconamide is also low in the blood of glaucoma paents and we have now demonstrated that niconamide treatment can increase visual funcon in glaucoma paents. NAD producon is an ideal target for drug discovery for glaucoma and we have now generated a number of novel drugs that target these processes. This research program will further these studies by designing and tesng new NAD-generang drugs with an aim to raise NAD in the rena and opc nerve. This will provide novel glaucoma treatments that are not reliant on, but can be used in combinaon with, exisng pressure lowering treatments.

THE KUMAR MAHADEVA GRANT AWARD 2021 - 2023Uncovering the Potenal of Pericytes as Therapeuc Targets for GlaucomaPrincipal Invesgator: Adriana Di Polo, PhD University of MontrealRenal ganglion cells (RGC), the neurons that die in glaucoma, are metabolically acve and require a precise regulaon of blood supply to meet their high oxygen and nutrient demand. The vascular theory of glaucoma proposes that insucient blood ow contributes to RGC neurodegeneraon. Glaucoma paents suer from vascular decits including decreased blood ow in the rena and opc nerve, reduced vessel caliber, and capillary defects. Notably, vascular autoregulaon and icker-induced neurovascular coupling, a key process that matches blood ow to the metabolic demand of acve neurons, are severely compromised in this disease. However, the cellular mechanisms underlying vascular dysfuncon in glaucoma and their impact on neuronal damage are currently unknown. Pericytes, the ensheathing cells that wrap around capillary walls, have emerged as key regulators of microcirculatory blood ow and neurovascular coupling. Pericytes are centrally posioned within the neurovascular unit, contain contracle proteins, and respond rapidly to neuronal smulaon. The renal microvasculature is rich in pericytes, with >90% pericyte coverage in human renal capillaries. We recently reported that inter-pericyte tunneling nanotubes (IP-TNTs), ne tubular processes that connect renal pericytes on distal capillary systems, are essenal for neurovascular coupling in the rena. These ndings were published in the impacul journal Nature (2020) and were lauded as crically important by the scienc community at large. Despite this, the role of pericytes and IP-TNTs in vascular dysregulaon in glaucoma has not been invesgated. To ll this knowledge gap, we recently developed a novel two-photon laser scanning microscopy (TPLSM) technique to visualize renal pericytes and single capillary blood ow in living mice).

Human Stem Cell Derived RGCs for Invesgang Nrf2 Acvaon as Neuroprotecon Approach in GlaucomaPrincipal Invesgator: Arupratan Das, PhDIndiana UniversityProgressive loss of renal ganglion cell (RGC) neurons of opc nerve causes glaucoma leading to complete blindness. Currently, over 3 million Americans are suering from glaucoma without any cure. Lowering high eye pressure provides temporary relief but without the cure. Till date no therapy is available for RGC neuroprotecon in glaucoma. Thus, there is a crical need to develop therapy to protect the RGC neurons. Studies in glaucoma paents’ rena and in animal models of glaucoma have widely found presence of elevated reacve oxygen species (ROS) which are toxic chemicals and cause oxidave stress, potenally leading to RGC death in glaucoma. Mitochondria are the energy source for cells, but damaged mitochondria are the primary source of toxic ROS chemicals. In healthy cells, ROS are cleared by acvaon of Nrf2 transcripon factor. Several of Nrf2 acvators are under FDA clinical trials for neurodegenerave diseases. Though ROS accumulaon observed in glaucoma paents’ rena, nothing is known if Nrf2 acvaon could remove ROS and protect human RGC neurons as a potenal therapy for glaucoma. In this proposal we will use human stem cell derived RGC neurons and test if Nrf2 acvaon could serve as neuroprotectant under glaucomatous condion.2021 RESEARCH GRANTS

Forecasng Glaucoma Progression and the Need for Surgical Intervenon using Arcial IntelligencePrincipal Invesgator: Linda Zangwill, PhD Sally Baxter, MD, MSc (Co-Principal Invesgator) Mark Christopher, PhD (Co-Principal Invesgator) Viterbi Family Department of Ophthalmology Shiley Eye Instute, Hamilton Glaucoma Ctr. UC San DiegoPrimary open angle glaucoma is a leading cause of blindness in the United States and worldwide. However, there is no way to predict in advance which individuals are at greatest risk of progressing to vision loss in paents who are diagnosed and then medically treated for glaucoma. Such paents might then be considered for surgical intervenon to delay vision loss. There have been important innovaons in arcial intelligence (AI) applicaons in healthcare, in general, and parcularly in ophthalmology. Although considerable progress has been made in developing AI algorithms to detect glaucoma using imaging and visual eld data, few have integrated these results in one model. Even fewer have incorporated informaon from clinical examinaons and electronic medical records to support clinical decision-making. This study is designed to address this important unmet need. The overall objecve of this proposal, “Forecasng Glaucoma Progression and the Need for Surgical Intervenon using Arcial Intelligence”, is to use mulmodal AI and deep learning strategies to predict which glaucoma paents will need glaucoma surgery. We will leverage exisng data from diverse research datasets and real-world clinical glaucoma populaons for the development and tesng of the deep learning models. Data from clinical examinaons, electronic health record data, opcal coherence tomography imaging and visual eld tesng will be used as input for the development and tesng of the AI algorithms that can predict which paents will likely need glaucoma surgery. 2021 -2022 RESEARCH GRANT IN AI

Linda Zangwill, Ph.D, is Professor of Ophthalmology and co-Director of Clinical Research and Director of the Imaging Data Evaluaon and Analysis (IDEA) Center at the Hamilton Glaucoma Center. Dr. Zangwill received her M.S. at the Harvard School of Public Health and her Ph.D. from Ben-Gurion University of the Negev.Dr. Zangwill’s research focuses on improving our understanding of the complex relaonship between structural and funconal change over me in the aging and glaucoma eye, developing computaonal and stascal techniques to improve glaucomatous change detecon, and idenfying risk factors that can predict rapidly progressing glaucoma.As Director of the Imaging Data Evaluaon and Analysis (IDEA) Center, Dr. Zangwill has developed and implemented protocols for ulizing diagnosc imaging instruments in naonal and internaonal mutli-center clinical trials of glaucoma and ocular hypertension.The three UCSD Principal Invesgators, Linda Zangwill, PhD, Sally Baxter, MD, MSc and Mark Christopher, PhD are joined by invesgators Robert N. Weinreb MD (UCSD), Christopher Girkin MD, MPH and Massimo Fazio, PhD (University of Alabama, Birmingham), and Jerey Liebman MD (Columbia University) to complete this important work. This proposal will build upon the prior work conducted by this research team to develop AI algorithms that incorporate a variety of data types to improve forecasng of clinical outcomes for glaucoma paents2021 -2022 RESEARCH GRANT IN AI

Elasc Fibers and Exfoliaon GlaucomaPrincipal Invesgator: Rachel W. Kuchtey, MD, PhDVanderbilt Eye InstuteExfoliaon glaucoma (XFG) is one of the most common types of secondary glaucoma, which will lead to irreversible blindness if le without treatment. In order to eecvely treat this disease, precise understanding of its molecular mechanisms is needed. The breakthrough genec discoveries over the last decade have paved the pathways leading toward our goal. LOXL1, encoding lysyl oxidase-like 1 protein is the most signicant gene associated with XFG and the interacon between lysyl oxidase-like 1 and brillin-1 has been increasingly recognized as they are two essenal elements for proper elasc ber formaon and funcon. We propose to use our newly created mouse model supported by The Glaucoma Foundaon during the rst funding cycle to invesgate the roles of those two molecules in XFG. If successful, new treatments could be quickly tested in our model in the near future.“As a glaucoma clinician, I have deep appreciation on how the disease impacts a patient’s life and I will draw great satisfaction when we can get the disease under control one patient at a time. However, my decade and a half experience in the clinic also tells me we need a permanent x. It is clear to me that only through in-depth basic science research can we make the cure of glaucoma possible.” 2021 RESEARCH GRANTS

New Tools to Understand Intraocular Pressure Regulaon at the Level of Aqueous Veins and Sclera ComplexPrincipal Invesgator: Guan Xu, PhDUniversity of MichiganA great proporon of paents with glaucoma, especially those with exfoliaon glaucoma that progresses rapidly, require surgical intervenon to avoid blindness. However, the lack of knowledge of how aqueous drainage paths behave when pressure in the eye uctuates is a crical barrier to the accurate predicon of surgical outcomes. The goal of this proposed project is to ll this knowledge gap using an advanced imaging technology combined with an established mechanical analysis method. In our preliminary study, we have already shown that our approach can resolve the deformaon of aqueous drainage paths and the surrounding ssue in the eye in 3 dimensions, which has not been achieved by any exisng technology. During the funding period, we will further validate our approach by comparison to standard ssue measurement tools. Aer the validaon, we will analyze the deformaon of the aqueous drainage path and their surrounding sclera under well-controlled pressure in pig eyes and human donor eyes. These analyses will provide us with the knowledge needed for selecng appropriate surgical procedures for the most desirable paent outcomes. 2022 RESEARCH GRANTS

The Role of Le-Right Determinaon Factor 2 (LEFTY2) in Exfoliaon GlaucomaPrincipal Invesgator: Steven Bassne, PhDWashington University School of MedicineExfoliaon glaucoma is a potenally blinding condion aecng millions of people worldwide. Unfortunately, paents are oen unaware of this disease unl a signicant poron of their vision has been lost irretrievably. One of the goals of this project is to determine whether the levels of a protein called LEFTY2 can be used to diagnose the condion or predict which paents are likely to be aected most severely. The study will also examine which cells produce LEFTY2 and its eect on cells in the drainage pathway of the eye.2022 RESEARCH GRANTS

JOE AND MARILYN ROSEN GRANTMolecular Mechanisms of Reacve Astrocyte Neurotoxicity to Human Renal Ganglion CellsPrincipal Invesgator: Xiz Chamling, PhDJohns Hopkins University School of MedicineGlaucoma, the second leading cause of blindness, has no therapeuc approaches available except for lowering intraocular pressure. Drugs that can protect renal ganglion cells (RGCs), the neuronal cells whose death leads to vision loss in glaucoma, is a potenal therapeuc opon to prevent vision loss. However, developing such drugs has been dicult because the cause of RGC death in glaucoma is not fully understood. Several studies are now suggesng that another cell type, called astrocytes, that populate the brain and opc nerve (bundle of nerves that connect the eye to the brain), can release toxic factors when they are stressed and not funconing normally. Such stressed astrocytes are called reacve astrocytes and the factors secreted by them can kill the RGCs. In our lab, we have established methods to convert human stem cells to human RGCs and human reacve astrocytes in a dish. Using these cells, we plan to study how reacve astrocytes cause RGC death. By studying the cause of human RGCs death, we hope to idenfy targets for developing drugs to protect RGCs and prevent glaucoma-related vision loss.

A Novel Transcripon Factor for Neurodegeneraon Therapy in Glaucoma and Opc NeuropathyPrincipal Invesgator: Kun-Che Chang, PhDUniversity of PisburghGlaucoma is the second leading cause of blindness worldwide, esmated to aect ~80 million people in 2020. So far there is no permeant therapy for glaucoma. However, vision restoraon through gene delivery strategies could be potenal soluons for such a disease. In this proposal, we idenfy a novel therapeuc gene and will apply it to a glaucomatous animal model, which will not only provide us a deeper understanding of the molecular mechanism of this gene in neuroregeneraon therapy but also a foundaon of the translaonal experiment forpreclinic study.2022 RESEARCH GRANTS

Opc Nerve Head Perfusion in a Murine Model of Pathological MyopiaPrincipal Invesgator: Rachel Shujuan Chong, MBBS, MMed(Ophth), PhDSingapore Eye Research InstuteMyopia is an important risk factor for glaucoma – high myopia in parcular has been suggested to increase the risk of developing this sight-threatening disease by 3 to 7-fold. Elongaon of the eyeball that occurs in myopia oen results in deformaon of structures in the eye, including the opc nerve head where glaucoma damage occurs. It is possible that myopia-associated changes to the eye shape also aects the blood vessels that supply renal ganglion cells at the opc nerve head, although this has not been studied in great detail to date.We aim to invesgate how myopia can alter blood vessel structure and funcon around the opc nerve head using state-of-the-art methods of ocular imaging and ssue analysis in a mouse model of high myopia that demonstrates similar characteriscs as human myopia. Our study will enable deeper insight into the mechanisms that underlie myopia-associated glaucoma, which may help clinicians to idenfy paents who are most at risk of losing sight in future.2022 RESEARCH GRANTS

The Genec Landscape of Blinding Exfoliaon GlaucomaPrincipal Invesgator: Chiea Chuen Khor, MB, BS, DPhilSingapore Eye Research InstuteExfoliaon syndrome is a major cause of irreversible blindness throughout the world. This condion was found to be heritable and accordingly, genec variants showing signicant associaons with risk of exfoliaon syndrome have been discovered. However, comparavely lile has been done to invesgate the potenal role of human genes and propensity for progression towards blinding exfoliaon glaucoma. We rst asked whether CYP39A1, a gene where carriers of mutaons had a 2-fold increased risk of exfoliaon syndrome, would also be involved in exfoliaon glaucoma-related blindness. We observed that persons with exfoliaon syndrome carrying a loss-of-funcon CYP39A1 variant have >7-fold risk of blindness compared to persons with exfoliaon syndrome who did not carry any CYP39A1 variant. When only paents with exfoliaon glaucoma were considered, carriers of CYP39A1 G204E were observed to have 5.9-fold increased risk of blindness compared to non-carriers. Although we were encouraged that genec variants conferring such high odds of blindness actually exist, the associaon with CYP39A1 only explained between 10 to 20 percent of blindness due to exfoliaon glaucoma. We hypothesize that addional genes could be involved in this irreversible, debilitang process. To address this queson, we propose to perform long read sequencing mapping and search specically for structural variants that are strongly associated with blindness. Structural variants has yet to be systemacally studied, and will be accessible using long-read sequencing. Data from this proposal has the potenal to uncover genec markers that may be useful for idenfying individuals at high risk of exfoliaon syndrome related blindness.2022 RESEARCH GRANTS

Biochemical Characterizaon of LOXL1 and Eect of Variants Associated with Exfoliaon SyndromePrincipal Invesgator: Raquel L. Lieberman, PhDGeorgia Instute of TechnologyExfoliaon syndrome (XFS) is a leading risk factor for secondary glaucoma, a major cause of blindness worldwide. Genec changes in LOXL1 were discovered in connecon with XFS 15 years ago, yet how the LOXL1 gene product contributes to disease is sll unknown. In this proposal we will use state of the art biochemical techniques to characterize LOXL1 and elucidate the changes that occur with genec changes proposed either to cause or prevent XFS. In the long term, this study will result in new insights into how LOXL1 contributes to XFS/XFG, as well as new direcons for therapeucs.2022 RESEARCH GRANTS

Role of LOXL1 Variants in Elasc Fiber FormaonPrincipal Invesgator: Dieter P. Reinhardt, PhDMcGill UniversityExfoliaon syndrome (XFS) manifests as excessive deposits of abnormal elasc ber proteins in various organs, especially in the eye where it can lead to blindness. XFS is linked to the LOXL1 gene giving rise to the enzyme lysyl oxidase-like 1 (LOXL1) which is responsible to polymerize elasc bers. Small changes in LOXL1 termed “variants”, can either promote or protect from XFS. The objecve of this proposal is to analyze the consequences of specic LOXL1 variants with either protecve or risk proles on the funcon and development of elasc bers. We will analyze the structure and aggregaon of these LOXL1 variants, their interacon with elasc matrix proteins, and their contribuon to elasc ber formaon. We expect from the results of this project to beer understand how LOXL1 variants can either promote or reduce the risk of geng XFS. The project may even open new avenues for therapies for XFS.THE HARRIET AND STANLEY SLOANE GRANT FOR EXFOLIATION GLAUCOMA RESEARCH-2022

Niconamide and Pyruvate for Neuroenhancement in Open-Angle Glaucoma: A Phase 2 Randomized Clinical TrialPrincipal Invesgator: Simon John PhDColumbia University Irving Medical Center Glaucoma is the leading cause of irreversible blindness worldwide. Themost important test to detect progression is visual eld tesng. Visual eldtesng is the reference standard to measure visual funcon in glaucoma. Itis called called standard automated perimetry (SAP). However, this test isvery subjecve, oen unreliable, and variable. One of the main causes ofunreliable tests is the lack of aenveness or concentraon during the test.Previous studies have shown that listening to Mozart or taking vitamin B12 canimprove the reliability of this test. Recent studies have suggested that over-the-counter medicaons such as niconamide (vitamin B3) and pyruvate canalso improve the performance during this test. This can ulmately reduce costsdue to repeated tesng and increase doctor’s certainty when analyzing theresults of this test. This study seeks to test whether these over-the-counternutrional supplements have an impact on paents’ performance during visualeld tesng.BARRY FRIEDBERG AND CHARLOTTE MOSS GRANT

Vascular Genotype-Phenotype Associaon in Primary Open Angle GlaucomaPrincipal Invesgator:Lucy Q. Shen, MDHarvard Medical School Current treatment opons for glaucoma only lower eye pressure, but some paents connue to lose vision from damage to their opc nerves. This means there are other causes of glaucoma. We found that the small blood vessels supplying the opc nerve in the eye are decient in paents with glaucoma. This deciency matchesthe loss of blood vessels in the ngers of glaucoma paents, suggesng that glaucoma is a disease aecng the blood vessels not only in the eye but also in the body. The reason for the inadequacies of blood vessels may be genecs. A number of genes can increase the risk of glaucoma, and some of these genes also aectblood vessels. In this study, we will use the paent’s genec informaon to evaluate the genes aecng blood vessels and assess the connecon between genec risk and blood vessel deciency in the opc nerve and in the body of paents with glaucoma. We hope to show that some paents are losing vision from glaucoma dueto decient blood vessels, and this is caused by their genec make-up. This may lead to new ways to treat glaucoma by targeng the blood vessels and the genes that control them. 2023 RESEARCH GRANTS

Invesgang the Role of Impaired Mitochondrial Dynamics in Exfoliaon GlaucomaPrincipal Invesgators: Audrey Bernstein, PhDArunkumar Venkatesan, PhDSUNY Upstate Medical UniversityExfoliaon glaucoma (XFG) is a more severe form of open angle glaucoma and a blinding disease. The eye starts accumulang white aky brillar aggregates blocking uid exit from the eye. As XFG is a mulfactorial disease, evidence suggests that the pathogenesis of the disease is associated with genec variants, environmental factors, protein aggregaon, oxidave stress, and cellular dysfuncon. This proposal aims to study defects in mitochondrial funcon in XFG paentderived primary cells and the relaonship of mitochondrial dysfuncon to cellular senescence (aging cells). Mitochondria are essenal cellular organelles that play crical roles in cellular energy metabolism and are known to be responsible for oxidave stress-induced damage in age-dependent neurodegeneraons such as glaucoma. Hence, maintaining mitochondrial health is evolving as a fundamental part of prevenng aging diseases. This study will evaluate how mitochondrial funcon is impaired in XFG and examine therapeuc strategies to enhance mitochondrial funcon for the treatment of XFG.THE GLAUCOMA FOUNDATION / BRIGHTFOCUS FOUNDATION GRANT AWARD-2023

2023 RESEARCH GRANTSSearch for Funconal LOXL1 Risk Alleles with BiT-STARR-seqJohn H. Fingert, PhDCarver College of MedicineUniversity of IowaExfoliaon glaucoma is a common cause of vision loss and disability that has a strong genec basis. One gene, lysyl oxidase like 1 (LOXL1), has an outsized inuence on risk for exfoliaon glaucoma, with an odds rao as high as 20. However, the specic genec variants in or near the LOXL1 gene that confer this risk for exfoliaon glaucoma remain unknown. The goal of our proposal is to use cung edge technology (BiT-STARR-seq) to test dozens of LOXL1 genec variants in parallel to rapidly determine which are the source of risk for exfoliaon glaucoma. These experiments and others will reveal the causes of exfoliaon glaucoma at the most basic molecular level and provide the informaon needed to build new, targeted, more eecve therapies to prevent vision loss.

2023 RESEARCH GRANTSRe-Purposing an “Old” Drug for a New Indicaon: Elucidang the Peripheral and Central Eects of Glucagon-Like Pepde 1 Receptor Agonists to Treat GlaucomaQi N. Cui, MD, PhDPerelman School of MedicineUniversity of PennsylvaniaGLP-1R agonists are a popular class of therapy for type 2 diabetes mellitus and weight loss. These drugs have demonstrated early promise as a novel treatment for glaucoma that does not rely on lowering intraocular pressure. This study, building upon previous ndings from our lab, will delineate the ocular, circulang, and central eects of GLP-1R agonists, and to test the ecacy of dierent formulaons of an FDA-approved GLP-1R agonist, Exendin-4, for treang glaucoma. This proposal will reveal protecve pathways behind not only glaucoma but other neurodegenerave processes and seeks to posively impact human eye health by revealing a novel therapy for a blinding disease.

2023 RESEARCH GRANTSUsing Arcial Intelligence to Reveal Blood Pressure’s Role in Glaucoma ProgressionAlon Harris, MS, PhD, FARVOIcahn School of MedicineOpen-angle glaucoma is a leading cause of irreversible blindness historically associated with elevated eye pressure. However, many paents develop glaucoma and experience its connued disease progression despite low or medically reduced pressures. The signicant connued disease burden demonstrates the high importance of nding new, non-invasive, and highly accessible diagnosc targets. High and low blood pressure as well as impaired blood ow and oxygenaon in eye ssues have also been linked to glaucoma. Using blood pressure to help improve diagnosis and paent care, however, has been dicult due to the complexity of unraveling and quanfying the impact of blood pressure on the eye’s circulaon and disease progression. We solve these challenges by combining validated cung-edge arcial intelligence techniques with novel data from early-stage open-angle glaucoma paents followed over me. Already, we have observed early-stage glaucoma paents to have specic vascular insult surrounding the eye’s nerve cells before experiencing any vision loss. The proposed research is highly relevant to public health because blood pressure is easy to measure, highly accessible, and when properly described with new arcial intelligence techniques will be able to clarify the role of blood pressure in glaucoma disease and promote improved methods to preserve vision worldwide.

Role of the Immunoproteasome in Glaucoma NeuroinammaonMarkus H. Kuehn, PhDThe University of IowaWhile elevated intraocular pressure is a strong risk factor for glaucoma other, pressure independent, disease mechanisms clearly contribute to vision loss in a large majority of paents. Our previous ndings, as well as those presented by other invesgators, have demonstrated that autoimmune reacons can develop during the disease resulng in slow but chronic vision loss. However, it is currently not clear how these immune reacons to become established in some paents. The immunoproteasome is a mul-enzyme complex that is crucial for the iniaon of immune responses. We propose to invesgate the role of the immunoproteasome in glaucoma using a mouse model of the disease. Highly specic inhibitors of this complex exist, and these have been shown to reduce damage in other neurodegenerave diseases. Consequently, demonstraon that acvaon of the immunoproteasome worsens glaucoma would provide strong support for the development of novel medical treatments aimed at preserving vision in glaucoma paents.2024 RESEARCH GRANTS

Advanced In Vitro Model for Pseudoexfoliaon Syndrome and GlaucomaUrsula Schlötzer-Schrehardt, PhDUniversity of Erlangen-NürnbergPseudoexfoliaon (PEX) syndrome is esmated to aect between 10 and 20% of people over the age of 60 and is frequently associated with a severe form of glaucoma that may account for over 25% of all open-angle glaucoma cases worldwide. Glaucoma in PEX paents is believed to result from accumulaon of an abnormal brillar matrix product (PEX material) in intra- and extraocular ssues. Currently there is limited informaon about the mechanisms leading to the producon of such material and there is no specic treatment to prevent its accumulaon in the eye. A major limitaon to develop specic therapies is the lack of experimental models, which are used to analyze disease mechanisms and to idenfy specic treatments to inhibit the producon of PEX material. Therefore, we have been invesgang the potenal of using cells from small iris ssue specimens rounely obtained during glaucoma surgery in PEX glaucoma paents to generate a cell culture model for the disease. Our preliminary results show that it is possible to replicate the formaon of an abundant extracellular matrix, which also contains the typical brillar PEX material. The objecve of the current applicaon is to use this cell culture model to evaluate the eects of various PEX-associated stress condions and metabolic factors on matrix producon in order to idenfy novel therapeuc targets. In addion, immortalized cell lines will be generated to provide consistency in experimental approaches and open an opportunity to use this model by invesgators in the eld. Availability of such model should open new avenues to understand the disease and develop specic treatments.2024 RESEARCH GRANTS

2024 RESEARCH GRANTSTargeng Primary Cilia Signaling for Glaucomatous Opc NeuropathyYang Sun, MD, PhDStanford UniversityGlaucoma damages the opc nerve, leading to a slow and permanent loss of eyesight. This occurs because the cells in the rena and opc nerve deteriorate over me. To preserve and potenally restore vision, sciensts are exploring the role of cilia in promong the growth of nerve cells and improving how the rena responds to light. Using a new method, researchers are studying live mice to understand how changes in eye pressure aect the cilia signaling of nerve cells in the rena. They hope this will shed light on how cilia could help protect the opc nerve from damage.

20

Evaluang Funconal Synaptogenesis by Transplanted Human Stem Cell Derived Renal Ganglion CellsPrincipal Invesgator, Thomas V Johnson, MD, PhD Johns Hopkins University School of MedicineWhile eye doctors have ways of slowing or prevenng vision loss from some opc nerve diseases, there are currently no treatments that can restore vision that has already been lost to opc neuropathy. The Johnson Lab aims to change that. We are interested in developing methods to transplant stem cell derived RGCs into the eye in vivo and in studying the survival and funconal integraon of cells into recipient neurorenal circuitry. Our goal is to improve survival and funconal renal integraon of transplanted RGCs by modulang both intrinsic molecular pathways within RGCs and extrinsic barriers within the renal microenvironment, in clinically relevant models of opc neuropathy in vivo. Ulmately, we aim to transformavely impact clinical and translaonal ophthalmology by developing the next generaon of therapies to actually reverse vision loss in potenally blinding diseases like glaucoma.THE RAJEN SAVJANI GRANT AWARD

THE RAJEN SAVJANI GRANT AWARDNew Strategies to Promote Renal Ganglion Cell Regeneraon andNeurorecoveryPrincipal Invesgator,Adriana Dei Polo, PhDUniversity of MontrealDr. Adriana Di Polo’s laboratory focuses on the pathobiology of renal ganglion cells, the neurons that convey visual informaon from the rena to the brain via their axons in the opc nerve. Loss of vision in glaucoma, the leading cause of irreversible blindness worldwide, is caused by the death of renal ganglion cells. At present, there is no cure for glaucoma and current treatments are oen insucient to stop disease progression. We seek to understand the mechanisms underlying renal ganglion cell death and to develop novel therapeucs to preserve and restore vision.Using pre-clinical models of acute and chronic opc nerve damage, Our lab seeks to idenfy molecular cues that control renal ganglion cell survival in the injured eye. We are also invesgang the role of reacve glia and vascular decits in glaucomatous neurodegeneraon.We seek to idenfy molecular cues that control renal ganglion cell survival and regeneraon in the injured eye. Using pre-clinical models of acute and chronic opc nerve damage, we are currently invesgang signals that regulate renal ganglion cell death, dendrite retracon and regrowth, axon degeneraon, synapc loss and dysfuncon. Our laboratory has been acvely involved in pre-clinical development of compounds currently in clinical trials for ophthalmological applicaons. The goal is to use this knowledge to develop clinically-viable strategies to enhance renal ganglion cell protecon and regeneraon in glaucoma.

THE KEN AND LINDA MORTENSONGRANT AWARDThis one-of-its-kind research project is designed to correlate genetic predisposition to glaucoma with actual ophthalmic outcomes. We have assigned everyone in two Biobanks - one at Mount Sinai and another at Mass General Brigham - a glaucoma genetic predisposition score. We invite subjects with the highest and lowest genetic risk scores for a 3-hour exam that includes visual field testing, imaging of the optic nerve with the latest technologies, and various measurements of eye size and shape. We also take extensive histories regarding diet, dental status, and female reproductive health because these factors may modify the relation between genetic predisposition to glaucoma and the actual development of the disease. When the NIH reduced funding for this project, we were faced with the possibility of reducing the number of people invited to participate. This grant allows us to identify associations between genetic risk and the development of glaucoma and to recognize critical dietary and lifestyle factors that might impact the genetic risk of developing glaucoma. Overall, we plan to recruit 400 subjects with a low genetic predisposition to glaucoma and another 400 with the highest propensity to glaucoma. The study has a high chance of moving the field of glaucoma forward. Genetic profiling could play a major role in effectively identifying glaucoma early, an important priority for The Glaucoma Foundation.Understanding the Clinical Impact of Cumulave Genec risk to GlaucomaPrincipal Invesgator,Louis R. Pasquale, MD, FARVOMount Sinai Health System

TGF Scientific Advisory Board Robert Ritch, MD, Co-ChairmanMedical Director, TGFShelley and Steven Einhorn Disnguished Chair Emeritus Professor of Ophthalmology EmeritusChief, Glaucoma Services EmeritusSurgeon Director EmeritusThe New York Eye & Ear Inrmary of Mount SinaiLouis Pasquale, MD, FARVO, Co-ChairmanShelley and Steven Einhorn Disnguished ChairSite Chair, Department of Ophthalmology, Mount Sinai Hospital Vice Chair, Translaonal Ophthalmology ResearchMount Sinai Healthcare SystemMichael Anderson, PhDProfessor, Dept., Molecular Physiology and Biophysics Carver College of Medicine Iowa Glaucoma Center, Instute for Vision ResearchTin Aung, MMed, FRCS, FRCOphth, FAMS, PhD Execuve Director, Singapore Eye Research Instute Deputy Medical Director (Research) & Senior Consultant, Glaucoma Dept, Singapore Naonal Eye Centre Professor, Dept of Ophthalmology, Yong Loo Lin School of Medicine, Naonal University of SingaporeAudrey Bernstein, PhDAssociate Professor, Center for Vision Research Department of Ophthalmology, SUNY Upstate Medical UniversityTerete Borrás, PhD Professor, Department of Ophthalmology Gene Therapy CenterUniversity of North Carolina School of Medicine Claude F. Burgoyne, MDGlaucoma ServicesSenior Scienst and Research DirectorOpc Nerve Head Research LaboratoryDevers Eye Instute & Research LaboratoriesAbbot Clark, PhDRegents Professor, Pharmacology & Neuroscience Execuve Director, North Texas Eye Research Instute University of North Texas Health Science CenterMiguel Coca-Prados, PhDProfessor (Adjunct) of OphthalmologyDepartment of Ophthalmology and Visual SciencesYale University School of MedicineJonathan G. Crowston, BSc, MBBS, PhD, FRCOphth, FRANZCOProfessor of OphthalmologyCentre for Vision Research Duke-NUS, Singapore Eye Research InstuteJohn Danias, MD, PhDProfessor and Interim ChairDepartment of OphthalmologyState University of New York - DownstateC. Gustavo De Moraes, MD, PhD, MPHAssociate Professor of OphthalmologyColumbia University Irving Medical CenterChief Medical Ocer, Ora Clinical, Inc.Adriana Di Polo, PhDProfessor in Neuroscience and OphthalmologyCanada Research Chair in Glaucoma and Age-Related NeurodegeneraonUniversity of MontrealJohn H. Fingert, MD, PhD, FARVOHadley-Carver Chair in GlaucomaProfessor, Department of Ophthalmology and Visual SciencesCarver College of Medicine, University of IowaDirector, Glaucoma Genecs LabInstute for Vision ResearchJerey L. Goldberg, MD, PhDProfessor and Chair, Department of OphthalmologyByers Eye Instute at Stanford UniversityNeeru Gupta, MD, PhD, MBA, FRCSC, DABOProfessor and Dorothy Pis ChairChief of Glaucoma, University of TorontoDepartments of Ophthalmology & Vision SciencesLaboratory Medicine and Pathobiology, Faculty of MedicineProfessor, Dalla Lana School of Public Health University of TorontoDirector, Roy Foss and Family Glaucoma LaboratoryKeenan Research Centre for Biomedical ScienceLi Ka Shing Knowledge InstuteSt. Michael’s Hospital, Toronto

Alon Harris, MS, PhD, FARVO Vice Chair of Internaonal Research and Academic Aairs Director of Ophthalmic Vascular Diagnosc & Research Program Professor of Ophthalmology Icahn School of Medicine, Mount Sinai Michael Hauser, PhDProfessor of Medicine and OphthalmologyDuke University Medical Center Senior ScienstSingapore Eye Research InstuteThomas V. Johnson III, MD, PhDThe Shelley & Allan Holt Assistant Professor of OphthalmologyAssistant Professor of Cellular and Molecular MedicineWilmer Eye Instute, Johns Hopkins UniversityPaul L. Kaufman, MDErnst H. Bárány Professor of Ocular PharmacologyDepartment Chair EmeritusDepartment of Ophthalmology & Visual SciencesSchool of Medicine & Public HealthUniversity of Wisconsin-Madison Uday B. Kompella, PhDProfessor Department of Pharmaceucal SciencesUniversity of Colorado DenverRichard K. Lee, MD, PhDWalter G. Ross Disnguished Chair in Ophthalmic ResearchAssociate Professor of Ophthalmology, Cell Biology, and Neuroscience Graduate ProgramBascom Palmer Eye InstuteUniversity of Miami Miller School of MedicineJerey M. Liebmann, MDShirlee and Bernard Brown Professor of OphthalmologyVice Chair, Department of OphthalmologyDirector, Glaucoma ServiceHarkness Eye InstuteColumbia University Medical CenterYutao Liu, MD, PhDAssociate Professor Cellular Biology & AnatomyGraduate StudiesAugusta UniversityFelipe Medeiros, MD, PhDProfessor of OphthalmologyJoseph A.C. Wadsworth Professor of OphthalmologyDuke University School of Medicine Colm O’Brien, FRCS, MDProfessor of OphthalmologyMater Misericordiae University HospitalDublin, IrelandDieter Reinhardt, PhDDisnguished James McGill ProfessorFaculty of Medicine and Health Sciences & Faculty of DenstryMcGill UniversityUrsula Schlötzer-Schrehardt, PhDProfessor, Department of OphthalmologyUniversity of Erlangen–NürnbergJoel S. Schuman, MD, FACSElaine Langone Professor & Vice Chair for Research, Department of OphthalmologyProfessor of Biomedical Engineering, Electrical & Computer Engineering, Neuroscience & Physiology, and Neural ScienceNYU Langone HealthW. Daniel Stamer, PhDJoseph A. C. Wadsworth Professor ofOphthalmologyProfessor of Biomedical EngineeringDuke UniversityErnst Tamm, MD, FARVOVice President for Research and Support for Emerging Academics, University of RegensburgProfessor and Chairman Instute of Human Anatomy & Embryology Gülgün Tezel, MDProfessorHarkness Eye InstuteColumbia University Medical Center

Janey L. Wiggs, MD, PhD, FARVOPaul Ausn Chandler Professor of Ophthalmology, Vice Chair for Clinical Research in OphthalmologyCo-Director, Glaucoma Center of ExcellenceHarvard Medical SchoolAssociate Director, Ocular Genomics InstuteAssociate Director, Howe LaboratoryAssociate Chief for Ophthalmology Clinical ResearchAssociate MemberBroad Instute of Harvard and MITSenior Scienst, Massachuses Eye and Ear Barbara Wirostko, MDClinical Adjunct Professor Ophthalmology/Visual Sciences Moran Eye Center, University of UtahAdjunct Professor , Dept. of BioengineeringUniversity of UtahTing Xie, PhDKerry Holdings Professor of ScienceChair Professor and the HeadDivision of Life ScienceHong Kong University of Science and TechnologyDonald J. ZackJohns Hopkins University School of MedicineINDUSTRY LIAISONSBaldo Scassella Sforzolini, MD, PhD, MBAGlobal Head of R&D GaldermaNaj Sharif, BSc (Jnt Hons), PhD, DSc, FARVO, FBPhSVice President, Global Alliances & External Research (GAER),Global Ophthalmology R&DSanten Inc. USA

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