With our aging population comes an ever-increasing incidence of Alzheimer’s disease (AD), and other age-related dementias. By the year 2050, there is forecast to be more than 13 million people living with AD in the USA, and new treatments are desperately needed to prevent this impending epidemic. There are currently no effective therapies for AD, with current clinical trials all attempting to directly target amyloid beta (Aβ) peptides thought to be the driver of neuronal degeneration. In the long term, scientists believe that we may have to use cocktails of drugs to effectively slow the disease, much as we now do for diseases such as HIV/AIDS. A new concept in AD research is that cellular processes regulating protein turnover (ie, the balance between protein synthesis and protein degradation) could be manipulated to prevent the build-up of the toxic Aβ peptides that cause neurological failure. In this work, we will be developing novel small molecules and peptides that we hope will enhance this protein turnover in neurons, and provide a starting point for designing new AD drugs.
See what research we fund.
- Brett Collins, PhDThe University of Queensland (Brisbane, Queensland, Australia)ID:A2018627SJuly 18, 2018Alzheimer'sStandard$191,034
- Xi-Qin Ding, PhDUniversity of Oklahoma Health Sciences Center (Oklahoma City, OK)
Age-related macular degeneration (AMD) is characterized by a progressive death of retinal pigment epithelium (RPE) cells in the central macular region of the retina and subsequent degeneration of light-sensitive neurons (photoreceptors). Oxidative stress/damage to the RPE is recognized as the core pathogenic lesion of the disease. In this project, we study the role of thyroid hormone in RPE oxidative stress/damage and investigate whether suppression of thyroid hormone activity protects RPE against oxidative damage.ID:M2018107Collaborators:Goldis Malek, PhDJuly 1, 2018 to June 30, 2020Macular DegenerationStandard$160,000
Elizabeth Anderson Award recipient.
- Rosario Fernandez-Godino, PhDMassachusetts Eye and Ear Infirmary, Harvard Medical School (Boston, MA)
Age-related macular degeneration (AMD) affects more than 2 million individuals in the US and it will reach 3 million by 2020. Current therapies can improve vision only in some patients with advanced AMD; unfortunately, there is no effective therapy that prevents disease progression in patients with early disease or genetic predisposition. My aim is to create a cell-based model to discover the primary mechanisms activated by the combination of aging and genetic variants in complement genes in patients with early AMD; so that drugs can be designed to stop these mechanisms before they lead to major damage and legal blindness.ID:M2018115July 1, 2018 to June 30, 2020Macular DegenerationStandard$160,000
This grant is made possible by the Ivan Bowen Family Foundation.
- Florian Sennlaub, MD, PhDInstitut de la Vision (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
- Sanjeev Kumar, MDCentre for Addiction and Mental Health (Toronto, Ontario, Canada)
Agitation and aggression affect majority of patients with dementia related to Alzheimer’s disease (AD). Medications used to treat these symptoms are associated with many side effects. In this study we will use magnetic brain stimulation to understand the mechanisms of agitation in AD dementia, and use a non-invasive brain stimulation technique called transcranial direct current stimulation (tDCS) to treat agitation. If successful, this study will lead to development of a safe and effective treatment for agitation in AD.ID:A2018667SCo-principal Investigators:Tarek Rajji, MD, FRCPC; Daniel Blumberger, MD, FRCPC; Zafiris J. Daskalakis, MD, PhD, FRCPC; Benoit H. Mulsant, MD, FRCPC; Bruce G. Pollock, MD, PhD; Reza Zomorrodi, PhD; Corinne E. Fischer, MD, FRCPCCollaborators:Nathan Herrmann, MD, FRCPCJuly 1, 2018 to June 30, 2021Alzheimer'sStandard$300,000
- Yuan Lei, PhDEye and ENT Hospital of Fudan University (Shanghai, China)
The most effective therapy for glaucoma is reducing eye pressure, but it is not understood how the pressure in the eye is regulated. MicroRNAs (miRNAs) are very small genetic sequences that can regulate the expression of many genes. In fact, a single miRNA is so powerful that it can modulate several genes. The aim of this project is to understand the role of a very important miRNA in regulating intraocular pressure (IOP). This may be a very effective new way to treat elevated eye pressure in glaucoma.ID:G2018112July 1, 2018 to June 30, 2020GlaucomaStandard$99,546
- 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
- Chi Luu, PhDCentre for Eye Research Australia (Centre for Eye Research Australia)
The protective properties of high-density lipoprotein (HDL), “good cholesterol”, have been studied extensively in cardiovascular conditions. Chronic inflammation modifies HDL (to dysfunctional HDL) and impairs its positive functional properties such as anti-oxidant and anti-inflammatory actions. Restoring HDL function has been shown to inhibit inflammation and oxidative stress, and in turn, reduces the risk of cardiovascular diseases in humans. Given that age-related macular degeneration (AMD), an eye condition that causes the loss of central vision, and cardiovascular disease share many common risk factors, we hypothesized that HDL functionality has a role in the development and progression of AMD. The overall aim of this research project is to explore the role and therapeutic benefit of HDL in AMD.ID:M2018144July 1, 2018 to June 30, 2020Macular DegenerationStandard$160,000
- Jessica Cooke Bailey, PhDCase Western Reserve University (Cleveland, OH)
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. We want to study glaucoma in the Amish, a group that is essentially a very large family. We think that by understanding glaucoma risk in the Amish, we can learn more about the genes and pathways that influence this disease. This knowledge will serve to better inform preventative and treatment strategies relevant to the millions of people throughout the world who will likely acquire glaucoma unless new ways of understanding disease risk and prevention are developed.ID:G2018042July 1, 2018 to June 30, 2020GlaucomaStandard$150,000
- 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'sPostdoctoral Fellowship$150,000