Understanding the genetic risk factors associated with Alzheimer’s disease (AD) is important for identifying and directing successful treatment strategies. Of these risks, a gene known as the triggering receptor expressed on myeloid cells 2 gene, or TREM2, appears to increase the risk for developing AD by altering inflammatory responses and mediating the accumulation of toxic amyloid-beta protein in the brains of experimental mouse models. We propose a strategy that can reduce TREM2 expression in the context of AD and will investigate pathology and inflammation in response to TREM2 loss. Our results will identify the role of TREM2 in AD and help direct future TREM2-targeted therapies for AD patients.
See what research we fund.
- Timothy Miller, MD, PhDWashington University School of Medicine (St. Louis, MO)ID:A2018169SCollaborators:Ionis PharmaceuticalsJuly 1, 2018 to June 30, 2021Alzheimer's DiseaseStandard$298,335
- F. Kent Hamra, PhDThe University of Texas Southwestern Medical Center (Dallas, TX)
Glaucoma is the world’s leading cause of irreversible blindness. This BrightFocus Foundation research grant will apply new technologies to make live Brown Norway rat models in the lab that express human genes that lead the rats to develop human-like forms of glaucoma. “Humanized” rat models generated by this project will be used by eye researchers to find new therapies that specifically neutralize the human glaucoma-causing genes, thereby preventing glaucoma in the rats. Therapies that prevent glaucoma from developing in the humanized rat glaucoma models will provide candidate therapeutics for battling glaucoma in humans.ID:G2018080July 1, 2018 to June 30, 2020GlaucomaStandard$149,764
- Florian Sennlaub, MD, PhDFondation Voir et Entendre (Paris, France)
It has recently been shown that patients with sleep apnea syndrome (SAS) suffer more frequently from age-related macular degeneration (AMD), 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 project to study immune cell activation and detrimental inflammation by hypoxia might help explain the association of sleep apnea with AMD, and also that of other diseases, such as Alzheimer 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 macular degeneration in the future.ID:M2018096July 1, 2018 to June 30, 2020Macular DegenerationStandard$160,000
- Robert W. Nickells, PhDUniversity of Wisconsin-Madison (Madison, WI)
In order for cells to function normally, they need to make connections with other cells and with their environment. Breaking these connections will cause death. We believe that retinal ganglion cells (RGCs) lose these connections after optic nerve damage and that this may be one of the important initiators of their death in glaucoma. Understanding the importance of the link between ganglion cell connections and ganglion cell death may help us develop ways to prevent this pathology in optic neuropathies like glaucoma.ID:G2018166July 1, 2018 to June 30, 2020GlaucomaStandard$150,000
Recipient of the Thomas R. Lee Award for Glaucoma Research.
- Yingbin Fu, PhDBaylor College of Medicine (Houston, TX)
Age-related macular degeneration (AMD) is a disease that blurs the sharp, central vision you need for everyday activities, such as seeing faces, reading, sewing, and driving. Advanced AMD can be classified into the dry form (gradual breakdown of the light-sensitive cells in the macula) and the wet form (leaky blood vessels growing under the retina). The current treatment for wet AMD is suboptimal, while there is no treatment available for dry AMD. We propose to develop a novel and effective treatment for both the wet and dry forms of AMD by using a protein called AIBP (apolipoprotein A-I binding protein).ID:M2018142July 1, 2018 to June 30, 2020Macular DegenerationStandard$160,000
This grant is made possible by support from The Helen Juanita Reed Award for Macular Degeneration Research.
- Cara Croft, PhDUniversity of Florida (Gainesville, FL)
Tau is one of the two major proteins (along with beta amyloid) that changes and then builds up in the brain in Alzheimer’s disease (AD) and how it is linked to brain cell death is still unclear. I keep small sections of mouse brain tissue alive in dishes and use viruses to make them develop the buildup of tau that is seen in AD patients. First, I will look at changes in these mouse brain tissues that have tau buildup, and those that do not, to see why or if brain cells die. I then hope to treat these brain tissues to either prevent or treat the buildup of tau in order to understand if we are able to treat humans with AD in a similar way.ID:A2018149FCollaborators:Nicholas Seyfried, PhDMentors:Todd Eliot Golde, MD, PhDJuly 1, 2018 to June 30, 2020Alzheimer's DiseasePostdoctoral Fellowship$150,000
- Ross Poché, PhDBaylor College of Medicine (Houston, TX)
The Müller glial cells (MGCs) within the retina of zebrafish and other non-mammalian vertebrates exhibit the remarkable ability to regenerate damaged retinal tissue, while mammalian MGCs cannot. This project aims to identify the cellular and molecular mechanisms functioning as an intrinsic block to mammalian MGC-mediated retinal regeneration. We will also determine whether bypassing this blocking mechanism results in mammalian retinal regeneration. Such a finding may lead to new clinical methods to prevent or reverse vision loss due to retinal injury or disease.ID:M2018022July 1, 2018 to June 30, 2020Macular DegenerationStandard$160,000
- Yuan Lei, PhDEye and ENT Hospital of Fudan University (Shanghai, China)
The most effective therapy for glaucoma is reducing eye pressure, but it is not understood how the pressure in the eye is regulated. MicroRNAs (miRNAs) are very small genetic sequences that can regulate the expression of many genes. In fact, a single miRNA is so powerful that it can modulate several genes. The aim of this project is to understand the role of a very important miRNA in regulating intraocular pressure (IOP). This may be a very effective new way to treat elevated eye pressure in glaucoma.ID:G2018112July 1, 2018 to June 30, 2020GlaucomaStandard$99,546
- Na Zhao, MD, PhDMayo Clinic Jacksonville (Jacksonville, FL)
Studies show that having the apolipoprotein E4 (APOE4) gene increases a person's risk for Alzheimer's diseases (AD). The persons who have AD and/or the APOE4 gene have problems with obtaining energy in their brain. Insulin is a drug that could help with the process of breaking down substances in the cells to obtain energy. Thus we would like to use animal models to look at whether insulin can rescue the brain energy in the animals that have AD and/or APOE4 gene. Our findings will be very useful in understanding how apoE4 impairs brain health and how we can use insulin as an effective treatment for AD.ID:A2018777FMentors:Guojun Bu, PhDJuly 1, 2018 to June 30, 2020Alzheimer's DiseasePostdoctoral Fellowship$150,000
- Wei Cao, PhDBaylor College of Medicine (Houston, TX)
Alzheimer’s disease (AD) is a devastating disease with no cure. Often, the brains of AD patients have ongoing inflammation that fuels the disease. This project will study a new family of cytokines (ie, proteins regulating the immune system) which we recently detected in AD brains. Our goal is to obtain knowledge about how inflammation worsens AD, and also to identify targets for effective treatments.ID:A2018377SCollaborators:Hui Zheng, PhDJuly 1, 2018 to June 30, 2021Alzheimer's DiseaseStandard$300,000