With rising life expectancies and an aging baby boomer generation, Alzheimer’s disease (AD) has become widespread and it is 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. 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.
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- Shermali Gunawardena, PhDSUNY Buffalo (Buffalo, NY)ID:A2018509SJuly 1, 2018 to June 30, 2021Alzheimer's DiseaseStandard$300,000
- Suchismita Acharya, PhDUniversity of North Texas Health Science Center at Fort Worth (Fort Worth, TX)
Glaucoma is a blinding disease and it is estimated that over 76 million people will be affected by this disease by 2020. It is associated with elevated eye pressure and progressive death of retinal ganglion cells (RGCs), as well as degeneration of the optic nerve head (which connects the brain to the eye). Nitric oxide (NO), a small gaseous molecule, is known to act as antioxidant, and is a key player in relaxing the smooth muscle cells and protecting damaged blood vessels. NO has the potential to reduce eye pressure, with high possibility of protecting the neural cells; however, free radicals generated during optic neuropathy may deplete nitric oxide bioavailability. Our group is working on discovering multi-functional small molecules that may be used for glaucoma treatment to decrease eye pressure and protect neurons, retinal ganglion cells from death.ID:G2018056July 1, 2018 to June 30, 2020GlaucomaStandard$150,000
- Dimitra Skondra, MD, PhDUniversity of Chicago (Chicago, IL)
Age-related macular degeneration (AMD), the leading cause of blindness in adults over 50, is a complex disease in which genetic risk and lifestyle factors like diet play important roles, but the mechanisms by which these factors interact remain a mystery blocking the development of a cure and of prevention measures. Gut microbiome (millions of microbes living in our gut) play a key role in human health and diseases like cancer, allergies, dementia, and asthma, and are significantly affected by diet and lifestyle factors.
The goal of this innovative proposal is to study if gut microbes could be the missing link that connects diet/lifestyle factors and AMD by investigating how changes in the microbes in the gut by diet affect AMD development. This approach will help uncover mechanisms causing AMD and could provide a new breakthrough insight into new treatments that work by changing our gut microbiome to prevent the leading cause of blindness in our community.ID:M2018042July 1, 2018 to June 30, 2020Macular DegenerationStandard$160,000
- 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
- Sara Gallant, PhDUniversity of Southern California (Los Angeles, CA)
The ability to selectively remember important information and ignore distraction is critical for optimal memory performance, particularly when we experience a stressful or emotionally arousing event that consumes attentional resources. Evidence suggests that the locus coeruleus (LC), the part of our brain thought to instigate these selectivity processes under arousing conditions, degrades in aging and Alzheimer’s disease (AD). Yet little is known about the relationship between the LC and cognitive function in these populations. The goal of this research is thus to address a novel and critical research question: to determine the role of the LC in facilitating memory selectivity and how its role may be altered in aging and AD.ID:A2018449FMentors:Mara Mather, PhDJuly 1, 2018 to June 30, 2020Alzheimer's DiseasePostdoctoral Fellowship$150,000
This grant is made possible in part by support from Alzheimer’s Los Angeles.
- Farid Rajabli, PhDUniversity of Miami, Miller School of Medicine (Coral Gables, FL)
The strongest risk gene identified for Alzheimer 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 people and AD risk genes. We will facilitate the discovery of ethnic-specific genes and genetic changes increasing the risk for AD. This approach will allow us to move a further step toward personalized and precision medicine.
ID:A2018556FMentors:Margaret A. Pericak-Vance, PhD; Gary W. Beecham Jr., PhDJuly 1, 2018 to June 30, 2020Alzheimer's DiseasePostdoctoral Fellowship$150,000
- Jessica Young, PhDUniversity of Washington School of Medicine (Seattle, WA)
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 us 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 molecular features. 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.ID:A2018656SCollaborators:Suman Jayadev, MDJuly 1, 2018 to June 30, 2021Alzheimer's DiseaseStandard$300,000
- 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
- Jeffery Vance, MD, PhDUniversity of Miami (Miami, FL)
ApoE is a gene that is the strongest risk factor for Alzheimer disease (AD), but African carriers of the risk form of ApoE get AD less frequently than European carriers of the same form of the gene. We have localized the area on the chromosome that contains the DNA change that is lowering the risk for AD in Africans. By using DNA sequence data from different populations, comparing the sequence differences, and then seeing how the differences affect DNA function, we will create a small list of potential "protective" changes, changes that can be tested in biological models. The purpose is to identify how the protective DNA change works in Africans, and use that information to develop a drug to reduce the risk to get AD.ID:A2018425SCo-principal Investigators:Margaret Pericak-Vance, PhD; Gary Beecham, PhD; Anthony Griswold, PhDJuly 1, 2018 to June 30, 2021Alzheimer's DiseaseStandard$300,000
- 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