Brightfocus Foundation

“A draft of the federal form 990 is distributed to the audit committee for review prior to being submitted to the internal revenue service. The draft federal form 990 is distributed early enough to provide each committee member with a reasonable amount of time for review and submission of questions or comments prior to the filing deadline. The final federal form 990 is distributed to each member of the full board of directors prior to being filed with the internal revenue service. The draft or final federal form 990 may be distributed in person, by regular mail, e-mail, or fax.”

“Brightfocus has all employees, officers, and directors agree to the code of conduct that includes adherence to the conflict of interest and implementation policy. Each board director, officer, and employee is required to complete a conflict of interest disclosure statement annaually. Employees meet annually with the brightfocus' chief compliance officer to review their conflict of interest statements, and give an annual conflict of interest compliance report to the board chair and vice chair. If a conflict is reported, it is then referred to the president/ceo and/or brightfocus' legal counsel and, if appropriate and necessary, then to the board of directors or its appointed committee for further action. The director's and officer's statements are reviewed by the brightfocus legal counsel. If a conflict is reported, it is then referred to the board of directors or its appointed committee for further action. At the time of the brightfocus discussion and decision concerning a conflict of interest, the conflicted party is not present in the meeting.”

“Brightfocus' board of directors has overall authority and responsibility for approving the annual budget which includes salary and benefits for all employees at every level including non-director officers and key employees. All pay adjustments are made on a yearly basis effective april 1st, the beginning of the brightfocus fiscal year. Before approving the compensation of the president/ceo, the board determines the total compensation to be provided by brightfocus to the president/ceo is reasonable in light of the position, responsibility and qualification of the position held including the result of an evaluation of prior performance for brightfocus, if applicable. The president/ceo is evaluated annually by the board of directors through the use of an in-depth goal attainment structure, (developed with advice from board source) that includes a self assessment and a board of directors assessment and evaluation against set goals, outcomes and deliverables. In addition, the board of directors periodically engages an outside consultant to obtain and consider appropriate data, including a salary survey, which includes information compiled from the federal form 990 of other organizations, concerning compensation paid to ceos in like circumstances. In making the determination, the board of directors shall consider total compensation to include the salary and value of all benefits provided by brightfocus to the individual in payment for services. At the time of the brightfocus board discussion and decision concerning the president/ceo's compensation, the president/ceo is not present in the meeting. The board shall set forth the basis for its decisions with respect to compensation in the minutes of the meeting at which the decisions are made, including the conclusions of the evaluation and the basis for determining that the individual's compensation was reasonable in light of the evaluation and comparability data. The president/ceo is charged with the setting of salaries of all other employees in accordance with a compensation structure and budget approved by the board of directors. The president/ceo and human resources review employee compensation and benefits that include key employees, by periodically engaging an outside consultant to conduct compensation and benefit benchmarking studies that include various regional and national non-profit compensation reports and surveys. Compensation deliberations and decisions include the review of self and supervisory evaluations of employee performance compared to set individual and organizational goals.”

“Brightfocus makes its governing documents including its articles of incorporation and bylaws, the federal form 1023, the 501(c)(3) letter of determination from the internal revenue service, conflict of interest policy, audited financial statements and federal form 990 available to the public upon request. In addition, the public also has access to the annual report, audited financial statements, the 501(c)(3) letter of determination from the internal revenue service, and federal form 990 on our website.”

“Brightfocus foundation drives innovative research worldwide and promotes awareness of alzheimer's, macular degeneration, and glaucoma. Our vision is living free from diseases of mind and sight. Collectively, 1 in 16 people over the age of 40 in the u.s. Has one of these diseases. Brightfocus has a proven track record of supporting the most innovative, early-stage research seeking better understanding, treatments, or, ultimately, a cure for these diseases. Since 1973, brightfocus has awarded more than $190 million in research grants to thousands of scientists around the world. Our research funding has led to major contributions to the understanding of these diseases and to the awarding of two nobel prizes. Brightfocus-supported findings are consistently cited by other scientists at twice the frequency as other research findings. Our funding acts as a catalyst in early-stage research. The brightfocus research programs are designed to provide initial funding for highly innovative experimental ideas. Due to the structured grant review and approval process, the research impact of brightfocus is very high. Most recipients of brightfocus funding go on to receive future grants from other sources that are 10 times larger than the original brightfocus award. This one thousand percent return on brightfocus investment speaks to our ability to identify promising research in its earliest stages and spawn future scientific discoveries. It is our firm belief that having the courage to invest in innovative ideas will lead to revolutionary approaches and life-saving breakthroughs. Indisputably, the world-class research identified and supported by brightfocus is more than promising: it is making a real contribution to revolutionary science in the fight to save mind and sight. Along with funding cutting-edge research to find cures to some of society's costliest diseases, brightfocus also provides free educational materials and support to hundreds of thousands of patients and families affected by these diseases nationwide. We base these educational materials off of the latest research findings. Brightfocus increases public awareness of alzheimer's, macular degeneration, and glaucoma, and communicates with thought leaders and elected officials about the importance of scientific research in these areas. Brightfocus' award-winning public service announcements (psa) have appeared on television, radio, and in print throughout the nation. Both make a plan today: get your eyes checked and now is the moment to stop alzheimer's disease powerfully seek to raise awareness and early detection, and similar messages have been delivered through donated print psa space in airports and train stations, as well as at pharmacies and supermarkets. In fiscal year 2018, these psa messages generated $13,658,057 in donated media services and garnered 1.3 billion impressions. Starting in february 2014, we launched brightfocus chats, a free, interactive monthly telephone forum that brings together patients and caregivers to learn from, and ask questions of, leading researchers and specialists on vision diseases. The chats are archived on our web site, with audio and print transcripts available in a number of accessible formats. We continue to increase our print publications, many in spanish, that provide helpful information to patients and caregivers, and regularly unveil new video and audio resources in conjunction with allies in the medical and scientific communities. We have expanded our written content of key research findings, promoting and sharing this information through our web site and social media platforms. Capitalizing on emerging use of data visualization, our brightfocus infographics easily and visually communicate information on alzheimer's, macular degeneration, and glaucoma. More specifically, each of these program areas mail awareness-raising materials to hundreds of thousands of households, with messages focusing on: - risk factors and symptom recognition”

“Notable projects include: a focus on an international biosample and brain bank for biomarker discovery for high risk alzheimer's groups; determining risk algorithms in middle age for alzheimer's in men and women; scientific exchanges; and better use of modern technologies, including mobile technologies and big data, to increase the speed of clinical trials and research progress. Additional information about specific projects is included in schedules f & i. Brightfocus is honored to have supported the early research of two eventual nobel prize winners: dr. Stanley prusiner and dr. Paul greengard, whose work has been instrumental to our current understanding of alzheimer's disease. Brightfocus continues its partnership with the academic journal "molecular neurodegeneration" as the official journal of the brightfocus foundation. The journal publishes technical papers related to neurodegeneration in the three disease areas. As an "open access" journal, there is no fee for readers, and all content is free of charge and easy to access. This open access ensures maximal reach of journal contents to scientists and care providers worldwide. Molecular neurodegeneration is currently the highest impact open access journal in the neurosciences. In addition to supporting cutting-edge research, alzheimer's disease research provides excellent resources on detecting, treating, and living with the disease. These are available in both print as well as on our website, www.brightfocus.org. Alzheimer's disease is the only cause of death among the top 10 in america without a way to prevent, cure, or even slow its progression. It is an irreversible degeneration of the brain that causes disruptions in memory, cognition, personality, and other functions and inevitably leads to death. More than 5 million americans aged 65 and older are thought to have alzheimer's disease today, and that number is expected to triple by midcentury.”

“In addition to supporting cutting-edge research, macular degeneration research provides excellent resources on detecting, treating, and living with this disease. These are available in both print as well as on our website, www.brightfocus.org. Age-related macular degeneration is a leading cause of vision loss in the united states. It destroys the macula, the part of the eye that provides sharp, central vision needed for seeing objects clearly. The most common eye condition in people age 60 and older, it can lead to vision loss in one or both eyes, making it difficult to recognize faces, drive a car, or read.”

“During the fiscal year ending march 31, 2018, ngr awarded $1,899,310 for 13 new projects. Details about specific projects are included in schedules f & i. In addition to supporting cutting-edge research, national glaucoma research provides excellent resources on detecting, treating, and living with the disease. These are available in both print as well as on our website, www.brightfocus.org. Glaucoma is a group of diseases that damage the eye's optic nerve and can result in vision loss and permanent blindness. More than 3 million americans age 40 and older have glaucoma. More than 60 million people in the world have the disease, and that number is expected to increase by as much as 20 million by 2020. With early detection and treatment, glaucoma often can be managed to protect eyes from more serious vision loss, but it is estimated that only half of the people living with glaucoma are aware that they have the disease.”

“Recoveries of prior year grants 361,983. Change in present value of grants 122,750.”

“Region: east asia & pacific (d) purpose of grant: alzheimer's disease research by yim lui carol cheung, phd, entitled: (a2018093s) recognition of retinal fingerprint for alzheimer's disease using deep learning approach. Investigator's summary: early detection of alzheimer's disease (ad) allows early intervention to its upstream pathology, which is more likely to prevent or delay cognitive decline as suggested by current evidence, yet current diagnostic method for early ad are not applicable to population-based screening. Being an extension of the brain, our eye is also affected by ad and eyes from subjects with ad exhibit a structural pattern that may be used as a "retinal fingerprint" for early detection. In this study, an artificial intelligence (ai) will "learn" these retinal patterns with deep learning methods and, after that, will be able to identify eyes from individuals with ad. This technique only requires a routine eye-check, and represents an inexpensive, non-invasive, efficient and accessible method for identifying who are more likely to have ad. Grant awarded: $300,000, the chinese university of hong kong, china. For more information, visit the brightfocus website: www.brightfocus.org/grant/a2018093s region: europe (d) purpose of grant: alzheimer's disease research by saima hilal, phd, entitled: (a2018165f) the clinical relevance of cortical cerebral microinfarcts in degenerative brain pathology such as alzheimer's disease. Investigator's summary: damage to the small vessels in the brain are one of the major cause of alzheimer's disease (ad). Adequate treatment is currently not available because the exact process behind this disease is still unknown. With this proposal, we aim to find the cause for ad by finding small strokes in the brain. This will help us understand why ad is so common in people with small strokes and will help create means to cure and prevent this disease. Grant awarded: $150,000, erasmus medical center, rotterdam, netherlands. For more information, visit the brightfocus website: www.brightfocus.org/grant/a2018165f region: east asia & pacific (d) purpose of grant: alzheimer's disease research by stephanie rainey-smith, phd, entitled: (a2018402f) improving sleep to prevent alzheimer's disease. Investigator's summary: alzheimer's disease (ad) is a terrible illness which damages the brain of many older people, causing them to stop thinking clearly, to stop remembering important information about themselves, their family and their life, and to start behaving differently; these problems get so bad that daily tasks such as driving, reading or finding the right words when speaking to someone become very difficult or impossible. We know that a particular protein builds up in the brain of a person with ad and that the brain becomes smaller, but we don't know how to slow or stop the disease. Some scientists believe that sleep is important, but more work is needed to understand whether 'how long and 'how well' someone usually sleeps changes how likely they are to get ad, or alters the speed at which the changes in the brain happen. This study will explore the relationship between sleep, memory and thinking, and changes in the brain, by investigating whether improved sleep (better and longer) causes better memory and thinking, slower protein build up in the brain and slows the shrinking of the brain, with the results of this project hopefully helping to find a way to slow or stop this horrible disease. Grant awarded: $149,998, edith cowan university, joondalup, western australia. For more information, visit the brightfocus website: www.brightfocus.org/grant/a2018402f region: east asia & pacific (d) purpose of grant: alzheimer's disease research by brett collins, phd, entitled: (a2018627s) stabilizing the retromer protein complex with molecular chaperones for alzheimer's and parkinson's diseases. Investigator's summary: with our aging population comes an ever-increasing incidence of alzheimer's disease (ad),”

“Region: east asia & pacific (d) purpose of grant: national glaucoma research by yuan lei, phd, entitled: (g2018112) the role of micro rna21 in regulating aqueous humor outflow. Investigator's summary: the most effective therapy for glaucoma is reducing eye pressure, but it is not understood how the pressure in the eye is regulated. Micro rnas are very small genetic sequences that can regulate the expression of many genes. In fact, a single micro rna is so powerful that it can modulate several genes. The aim of this project is to understand the role of a very important micro rna namely micro rna21 in regulating iop. This may be a very effective new way to treat elevated eye pressure in an eye disease called glaucoma. Grant awarded: $99,546, eye and ent hospital of fudan university, shanghai, china. For more information, visit the brightfocus website: www.brightfocus.org/grant/g2018112 region: europe (d) purpose of grant: macular degeneration disease research by florian sennlaub, md, phd, entitled: (m2018096) influence of chronic intermittent hypoxia on neuroinflammation in age related macular degeneration. Investigator's summary: it has recently been shown that patients with sleep apnea syndrome (sas) suffer more frequently from age-related macular degeneration, but the reason for the association of both diseases remains obscure. Our preliminary data suggest that the episodes of hypoxia that characterize sleep apnea, activate circulating immune cells and lead to longer and stronger detrimental inflammation in the eye in amd models. Our proposal to study immune cell activation and detrimental inflammation by hypoxia might help explain the association of sleep apnea with amd, but also of diseases such as alzheimer's disease that are associated with sas and harmful inflammation. Increased awareness of this mechanism will help to diagnose and treat sas in affected amd patients, reducing their need for intra-vitreal injections and slowing the degeneration in the future. Grant awarded: $160,000, institute de la vision, paris, france. For more information, visit the brightfocus website: www.brightfocus.org/grant/m2018096 region: east asia & pacific (d) purpose of grant: macular degeneration research by chi luu, phd, entitled: (m2018144) reconstituted high density lipoprotein (rhdl) for the treatment of age-related macular degeneration (amd). Investigator's summary: in this project, we will examine the role of cholesterol on the development and progression of amd, an eye condition that causes the loss of central vision. We will also investigate whether amd can be treated with "good cholesterol." the findings from this project will pave the way for the development of new therapies for the management of the earliest changes in amd to prevent vision loss. There are no treatment options currently available for the early stages on amd to prevent its progression to vision loss. Grant awarded: $160,000, centre for eye research australia, east melbourne, australia. For more information, visit the brightfocus website: www.brightfocus.org/grant/m2018144”

“Name of organization or government: northwestern university. (h) purpose of grant: alzheimer's disease research by congcong he, phd, entitled: (a2018100s) mechanisms of autophagic regulation of a-beta metabolism against alzheimer's disease. Investigator's summary: autophagy, the pathway a brain cell uses to dispose of damaged structures inside the cell, is impaired in alzheimer's disease (ad). Brain cells produce amyloid, a toxic peptide that causes ad. Our research will show how activated autophagy can recognize and clear amyloids in different types of brain cells, and how to increase the activity of this pathway to accelerate the disposal of amyloids. For more information, visit the brightfocus website: www.brightfocus.org/grant/a2018100s name of organization or government: washington university. (h) purpose of grant: alzheimer's disease research by chao wang, phd, entitled: (a2018128f) ldlr-targeted therapy for apoe-related tauopathy. Investigator's summary: tau protein aggregation in neurons is one of the hallmarks for 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. For more information, visit the brightfocus website: www.brightfocus.org/grant/a2018128f name of organization or government: university of florida. (h) purpose of grant: alzheimer's disease research by cara croft, phd, entitled: (a2018149f) understanding and targeting tau-induced neurodegeneration. Investigator's summary: tau is one of the two major proteins that changes and then builds up in the brain in alzheimer's disease and how it is linked to brain cell death is still unclear. Using a mouse alzheimer's-in-a-dish model similar to the ad diagnosed in patients, the researchers will try to understand why some people have buildup of tau and others don't. Then they will treat the tissues to try and prevent the tau buildup. This will help us understand if we are able to treat humans with ad in a similar way. For more information, visit the brightfocus website: www.brightfocus.org/grant/a2018149f name of organization or government: washington university. (h) purpose of grant: alzheimer's disease research by timothy miller, md, phd, entitled: (a2018169s) antisense-mediated trem2 knockdown to lessen amyloid and tau pathology. Investigator's summary: 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 involved in inflammatory responses (trem2) increases risk for developing ad and appears to mediate the accumulation of toxic protein amyloid beta in the brains of mice with ad. 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. For more information, visit the brightfocus website: www.brightfocus.org/grant/a2018169s name of organization or government: university of miami, miller school of medicine. (h) purpose of grant: alzheimer's disease research by holly cukier, phd, entitled: (a2018197s) elucidating the cell-specific roles of abca7. Investigator's summary: alzheimer's disease (ad) occurs more frequently in diverse populations (i.e.: african americans and hispanics) than 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”

“Name of organization or government: sanford-burnham prebys medical discovery institute. (h) purpose of grant: alzheimer's disease research by yingjun zhao, phd, entitled: (a2018214f) targeting synaptic and memory deficits in alzheimer's disease. Investigator's summary: alzheimer's disease (ad) is the most prevalent neurodegenerative disorder world-wide, and has devastating effects on memory and brain function in afflicted patients. Although the exact causes that accelerate memory loss during aging is not known, it is likely that a toxic protein a-beta plays a vital role in disrupting communication junctions in the brain as ad progresses. Our goal is to understand how newly-discovered proteins that are overproduced in ad, can alter the brain to disrupt communication between neurons to cause problems with memory. By understanding changes behind memory loss in alzheimer's, we can begin to formulate strategies to restore neuronal connections and memories in aged ad patients. For more information, visit the brightfocus website: www.brightfocus.org/grant/a2018214f name of organization or government: icahn school of medicine at mount sinai. (h) purpose of grant: alzheimer's disease research by mickael audrain, phd, entitled: (a2018253f) microglial tyrobp involvement in tau propagation and associated inflammation. Investigator's summary: neuroinflammation in the brain has causes such as neurodegenerative diseases including diseases called "tauopathies". 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 tyrobp as a causal regulator controlling the garbage disposal actions of microglia. To elucidate 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 modify inflammation and the tauopathy progression and thereby greatly influence this field of research. For more information, visit the brightfocus website: www.brightfocus.org/grant/a2018253f name of organization or government: the salk institute for biological studies. (h) purpose of grant: alzheimer's disease research by weiwei fan, phd, entitled: (a2018325s) targeting ppar delta in alzheimer's disease. Investigator's summary: ppar delta is a protein that is present in the brain. It is suggested to have important functions in brain. This proposal will help us understand its exact functions in brain. I will also test whether we can target ppar delta to treat alzheimer's disease (ad). For more information, visit the brightfocus website: www.brightfocus.org/grant/a2018325s name of organization or government: washington university. (h) purpose of grant: alzheimer's disease research by celeste karch, phd, entitled: (a2018349s) cxcr4 as a modifier of tau aggregation in alzheimer's disease. Investigator's summary: several lines of evidence suggest that inflammation and altered function of the cell types in the brain involved in inflammation, such as microglia, represents an early and critical driver of alzheimer's disease (ad). Our group has recently shown that a chemokine receptor cxcr4 found in the cell types that mediate inflammation in the brain, such as microglia, contribute to tauopathies such as progressive supranuclear palsy, frontotemporal dementia, corticobasal degeneration, and alzheimer's disease. 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. For more information, visit the brightfocus website: www.brightfocus.org/grant/a2018349s name of organization or government: university of california, san francisco. (h) purpose of grant: alzheimer's disease research by ale”

“Name of organization or government: the research foundation for suny on behalf of university at buffalo sponsored projects services. (h) purpose of grant: alzheimer's disease research by shermali gunawardena, phd, entitled: (a2018509s) a novel therapeutic nano-vesicle for the clearance of axonal blocks to prevent alzheimer's disease. Investigator's summary: with rising life expectancies and an aging baby boomer generation, alzheimer's disease (ad) has become one of the leading causes of death in the u.s. Treating ad has proven difficult as current treatments are only able to target the late stage of disease with many adverse side effects and currently, there are no cures for ad. The challenge is to develop treatments that are able to specifically target affected neurons at early stages of disease initiation. We will use a highly innovative approach to develop synthetic biomolecules that will deliver therapeutics to specific sites within the brain, to modify defects that activate disease pathways. For more information, visit the brightfocus website: www.brightfocus.org/grant/a2018509s name of organization or government: university of miami, miller school of medicine. (h) purpose of grant: alzheimer's disease research by farid rajabli, phd, entitled: (a2018556f) evaluating the role of race, ethnicity, and genetic ancestry in alzheimer disease-associated genes. Investigator's summary: the strongest risk gene identified for alzheimer's 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 and ad risk genes. We will facilitate the discovery of ethnic specific genetic genes increasing the risk for ad. This approach will allow us to move a further step toward personalized and precision medicine. For more information, visit the brightfocus website: www.brightfocus.org/grant/a2018556f name of organization or government: university of washington school of medicine. (h) purpose of grant: alzheimer's disease research by jessica young, phd, entitled: (a2018656s) probing the role of the endocytic network in alzheimer's disease using human neuronal models. Investigator's summary: alzheimer's disease (ad) is a devastating neurodegenerative disorder that is the most common cause of dementia in the elderly and is a tremendous socioeconomic burden. Stem cells derived from human patients can help discover new therapeutics for ad because individual genetic background is captured in a dish and stem cells can be differentiated into neurons, a relevant cell type to analyze molecularfeatures. My proposal will test whether genes identified with ad risk confer measurable laboratory read-outs characteristic of ad in neurons grown in the laboratory. In particular, i will focus on a particular cellular pathway, the endosomal network, which may become dysfunctional in ad before amyloid and tau deposition are reported. For more information, visit the brightfocus website: www.brightfocus.org/grant/a2018656s name of organization or government: regents of the university of california, los angeles. (h) purpose of grant: alzheimer's disease research by daniel geschwind, md, phd, entitled: (a2018700s) a multi-level understanding of glial signaling in neurodegenerative tauopathy using integrative transcriptomic network analysis. Investigator's summary: recent scientific discoveries suggest that multiple cell types might participate in alzheimer's disease and understanding the key players and t”

“Name of organization or government: washington university. (h) purpose of grant: alzheimer's disease research by jeremy strain, phd, entitled: (a2018817f) white matter hyperintensity localization and severity in association with pet tau in alzheimer disease. Investigator's summary: each of the aims of this project are directed at understanding how and where structural connections in the brain are damaged in two variants of alzheimer's disease (ad). We discuss two known causes of white matter damage commonly seen in this population that can be detected by combining different neuroimaging and analytical techniques that we are capable of performing. This will improve our understanding of the biological correlates that characterize this disease and the subtle differences in progression between these two types of ad. For more information, visit the brightfocus website: www.brightfocus.org/grant/a2018817f name of organization or government: icahn school of medicine at mount sinai. (h) purpose of grant: alzheimer's disease research by edoardo marcora, phd, entitled: (a2017458s) understanding the role of apolipoprotein e in microglia. Investigator's summary: supplemental funding on award with non-tech abstract: human genetic studies strongly point to apolipoprotein e (apoe) and microglia (the immune cells of the brain) as, respectively, the most important gene and cell type in the chain of events that leads to alzheimer's disease (ad), a common disorder in the elderly in which the brain is damaged and memories falter. In normal conditions, microglial cells do not make apoe; however, in disease conditions, they sense the brain damage and respond by churning out apoe. It is unclear why this occurs and the goal of this project is to answer this question by investigating what happens to mice without the apoe gene in their microglia after they experience brain stress. For more information, visit the brightfocus website: www.brightfocus.org/grant/a2017458s name of organization or government: human computation institute. (h) purpose of grant: alzheimer's disease research by pietro michelucci, phd, entitled: (ca2017606) crowd powered microvascular modeling phase 2. Investigator's summary: the central aim of this project is to accelerate research into potential alzheimer's treatments targeting the brain microvasculature. This will be done through our eyeonalz project, which uses citizen science (a form of crowdsourcing). Without this crowdsourced program, the same research would otherwise take decades to complete. Our approach is to transform a time-consuming laboratory task into an online game that anyone can play. Project success depends upon recruiting and sustaining an active population of public volunteers and improving our ability to extract research value from each participant. We also hope this project provides a hands-on way for people affected by alzheimer's disease (ad) to make an impact on their own future or that of a loved one, and that it educates the general public about the disease. To learn more about eyesonalz, visit www.eyesonalz.com. Name of organization or government: human computation institute. (h) purpose of grant: alzheimer's disease research by pietro michelucci, phd, entitled: (ca2016629) crowd-powered microvascular modeling. Investigator's summary: additional funding for the fy16 award: cornell university researchers have made breakthrough discoveries in understanding the role of brain blood flow in alzheimer's disease (ad), but more evidence is needed to establish whether freeing stalled capillaries might results in a possible treatment approach. The problem is that it takes an entire year to analyze the data needed to answer each research question, and progress to date has been very slow. "stall catchers" is a citizen science research project developed by the human computation institute in collaboration with cornell investigators chris schaffer and nozomi nishimura aimed at speeding up cornell's data analysis by”

“Name of organization or government: massachusetts general hospital. (h) purpose of grant: alzheimer's disease research by jill goldstein, phd, entitled: (ca2018607) development of clinical algorithm to identify risk for alzheimer's disease in early midlife. Investigator's summary: 18% of the u.s. Is greater than 60 years of age, with projections of 25-30% by 2050. Thus, healthy aging is one of the most important public health challenges of our time. Maintaining intact cognitive function is critical to that end. Most work on cognitive aging and alzheimer's disease (ad) begins with people greater than 65 years. However, we now know that successful treatment likely should begin in early midlife. We have an unprecedented opportunity to create a "living laboratory" for the identification of biomarkers and targets for therapeutics to enhance one's resilience to aging and prevent decline in cognition and other organ functions beginning in early midlife. We are leveraging the partners healthcare biobank by creating the bwh healthy aging translational cohort (hatch). This cohort is being created as a platform that would provide a research and clinical infrastructure for the study of disorders of aging, creating substantial opportunities investigators and industry partners with critical implications for precision medicine and healthcare utilization. Here, we propose to develop and validate a quantitative tool, a clinical risk algorithm, that integrates polygenic-clinical-physiological and neural phenotyping to identify in early midlife (ages 45-65 years) people who may already have accumulated amyloid pathology and are at highest risk for cognitive decline and ad later in life. For more information, visit the brightfocus website: www.brightfocus.org/grant/ca2018607 name of organization or government: oregon health and science university. (h) purpose of grant: national glaucoma research by benjamin sivyer, phd, entitled: (g2018011) axo-somatic and dendritic plasticity in glaucoma. Investigator's summary: glaucoma is a disease that causes the death of retinal cells that communicate with the brain. We have little knowledge of how this gradual process of cell death is influenced by other cells in the retina and gaining insight into these mechanisms will allow us to develop new ways to treat glaucoma. For more information, visit the brightfocus website: www.brightfocus.org/grant/g2018011 name of organization or government: case western reserve university. (h) purpose of grant: national glaucoma research by jessica cooke bailey, phd, entitled: (g2018042) glaucoma evaluation in the amish. Investigator's summary: 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 including (i) the specific type of glaucoma they have, (ii) they are unrelated and therefore their genetic backgrounds are complicated, and (iii) their environmental exposures vary widely. We want to study glaucoma in the amish, a group that is essentially a very large family, because (i) they are more likely to have the same type of glaucoma, (ii) their genetic backgrounds are more related, and therefore there is less confusing genetic 'noise' to sift through when performing genetic analyses, and (iii) they have fairly uniform lifestyles and therefore there environmental exposures are more similar to one another as compared to other groups in which glaucoma has been studied. We will examine their eyes, get detailed medical histories, ask many questions about their environmental exposures and lifestyle choices, and get blood so we can study their genetics. We think that by understanding glaucoma risk in the amish, we can learn more about the genes and pathways that influence this disease and apply this knowledge to better inform preventative and treatment strategies relevant to the millions of people throughout the world who will likely develop glaucoma without new ways of understanding disease r”

“Name of organization or government: university of tennessee health science center. (h) purpose of grant: national glaucoma research by monica jablonski, phd, entitled: (g2018116) new glaucoma models mined from an inbred genetic reference panel. Investigator's summary: millions of people are affected by glaucoma and some lose their vision due to this disease. To develop new drugs to treat glaucoma or to understand why glaucoma causes vision loss, it is important to have accurate models of the disease. Unfortunately, there are not enough models available that truly reflect the human disease. We hope to change that. In our study, we will identify and characterize new glaucoma models that share the disease phenotype of humans. These models will be a very useful resource for all vision scientists. For more information, visit the brightfocus website: www.brightfocus.org/grant/g2018116 name of organization or government: university of miami, miller school of medicine. (h) purpose of grant: national glaucoma research by xiangrun huang, phd, entitled: (g2018148) spectral contrast of retinal nerve fiber layer reflectance: a new means for sensitive detection of glaucomatous damage. Investigator's summary: 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 of 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. For more information, visit the brightfocus website: www.brightfocus.org/grant/g2018148 name of organization or government: university of wisconsin-madison. (h) purpose of grant: national glaucoma research by robert w. Nickells, phd, entitled: (g2018166) the pathological contribution of cell adhesion disruption in rgc death. Investigator's summary: 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 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. For more information, visit the brightfocus website: www.brightfocus.org/grant/g2018166 name of organization or government: university of illinois at chicago. (h) purpose of grant: national glaucoma research by biji mathew, phd, entitled: (g2018168) novel cell-free treatment of glaucoma. Investigator's summary: retinal ganglion cell death and axonal loss are hall mark events leading to glaucoma and, neuroprotection of retina by regeneration, or prevention of cells from dying, are key factors and major public health necessities. Our objective is to study the use of extracellular vesicles (ev), tiny particles secreted by mesenchymal stem cells, as a treatment for glaucoma induced cell death. Delivering the ev specifically into the retina and prolonging the effect, are major limitations reducing the treatment efficacy. Therefore, our study is focused to engineer modified targeted ev for retina-specific neuroprotective action for treating glaucoma. For more information, visit the brightfocus website: www.brightfocus.org/grant/g2018168 name of organization or government: university of akron. (h) purpo”

“Name of organization or government: the schepens eye research institute. (h) purpose of grant: macular degeneration research by magali saint-geniez, phd, entitled: (m2018064) investigation of a new target in age-related macular degeneration. Investigator's summary: central vision loss has a profound impact on the quality of life and functional ability of affected patients. In age-related macular degeneration (amd), such loss is attributed to the dysfunction of a layer of pigmented cells called the retinal pigment epithelium (rpe). The overarching goal of this project is to characterize the role of a protein, known to regulate the metabolic activity in cells, in amd pathogenesis and to offer critical validations to current clinical data associating this protein to the more advanced and blinding form of the disease, neovascular amd. Results from this work are significant not only to understand amd pathogenesis but also to open up new therapeutic options for the treatment of common retinal diseases. For more information, visit the brightfocus website: www.brightfocus.org/grant/m2018064 name of organization or government: university of texas southwestern medical center. (h) purpose of grant: macular degeneration research by john hulleman, phd, entitled: (m2018099) small molecule-based conditional control of inflammation and complement activation in the retina. Investigator's summary: this project seeks to determine whether dampening inflammation using a newly developed strategy can prevent a prevalent, currently untreatable inherited eye disease, stargardt disease. Our approach is unique in that it can be 'turned on or 'turned off' in the eye when necessary, thereby minimizing potential detrimental 'off target' effects associated with current similar strategies. We anticipate that this unique aspect of our strategy will make it more likely to be effectively used ultimately in humans with stargardt disease. For more information, visit the brightfocus website: www.brightfocus.org/grant/m2018099 name of organization or government: university of oklahoma health sciences center. (h) purpose of grant: macular degeneration research by xi-qin ding, phd, entitled: (m2018107) thyroid hormone signaling regulation of retinal pigment epithelium viability. Investigator's summary: age-related macular degeneration (amd) is an eye disease marked by progressive death of retinal pigment epithelium cells (rpe) and light-sensitive neurons (photoreceptor cells) in the central (macular) area of the retina. The disease is the leading cause of blindness in the elderly, and there are currently no curative treatments. Thyroid hormone (th) regulates cell growth, differentiation, and metabolism, and has recently been associated with increased risk of amd. This study will investigate the th regulation of rpe viability and determine whether suppressing th signaling protects rpe against oxidative damage. For more information, visit the brightfocus website: www.brightfocus.org/grant/m2018107 name of organization or government: university of miami, miller school of medicine. (h) purpose of grant: macular degeneration research by william scott, phd, entitled: (m2018112) genetic factors accelerating progression to advanced amd. Investigator's summary: age related macular degeneration (amd) is the leading cause of irreversible blindness in older adults in the u.s. 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. For more information, visit the brightfocus website: www.brightfocus.org/grant/m2018112 name of orga”

“Name of organization or government: helen keller foundation for research & education. (h) purpose of grant: 2017 helen keller prize for vision research partnership. The helen keller prize for vision research recognizes significant accomplishments in vision research, and provides funds for continuance of those studies. Name of organization or government: helen keller foundation for research & education. (h) purpose of grant: 2018 helen keller prize for vision research partnership. The helen keller prize for vision research recognizes significant accomplishments in vision research, and provides funds for continuance of those studies. Name of organization or government: dean mcgee eye institute. (h) purpose of grant: 16th international symposium on retinal degeneration 2018 meeting - exists to facilitate knowledge sharing amongst researchers in the amd community and other retinal disorders. Name of organization or government: scheie eye institute university of pennsylvania. (h) purpose of grant: macular degeneration research by benjamin kim, md, entitled: (cm2016971) therapeutic evaluation of alpha lipoic acid for geographic atrophy. Investigator's summary: supplemental funding on award with non-tech abstract: the blinding lesions of the geographic atrophy (ga) form of advanced age-related macular degeneration (amd) are responsible for 20 percent of the legal blindness in north america. Research has shown that oxidative stress and iron overload at the retina are major contributors to these atrophic lesions in amd, consisting of localized areas of dead cells. Currently there is no treatment available; however, there is interest in a potent antioxidant and iron chelator called alpha lipoic acid. A chelating agent is a substance whose molecules can form several bonds to a single metal ion, thus suppressing its chemical activity. Alpha lipoic acid is found in many food sources, including spinach, broccoli, and potatoes; it also is manufactured for use as a supplement. Through a phase ii pilot clinical trial, we are testing alpha lipoic acid as a treatment for ga. For more information, visit the brightfocus website: www.brightfocus.org/grant/cm2016971”