Alzheimer’s disease (AD) is linked to proteins that misbehave and stick together into protein particles that are toxic to brain cells. Early detection of this dreaded disease requires the generation of imaging molecules that can enter the brain and selectively tag the toxic protein particles in different parts of the brain. We aim to use an innovative design and evolution method for generating imaging probes specific for particles of one of the most harmful Alzheimer’s proteins (tau). We will use these novel probes to image toxic tau protein particles in the brains of mice used as models of AD, with the long-term goal of translating this technology to humans for early and accurate disease detection.
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- Peter Tessier, PhDUniversity of Michigan (Ann Arbor, MI)ID:A2017395SSeptember 1, 2017 to August 31, 2020Alzheimer'sStandard$300,000
- Daniel Bos, PhDErasmus Medical Center (Rotterdam, Netherlands)
Atherosclerosis, or hardening of the arteries, is increasingly recognized as an important risk factor for dementia. Yet, it remains unclear whether the progression of atherosclerosis at different locations in the arterial system also contributes to changes in the structure or function of the brain, and ultimately to dementia. Knowledge of the dynamics of atherosclerosis and its role in brain changes will greatly improve our insight into the development of dementia. At a later point, this knowledge may even offer therapeutic or preventive opportunities to reduce the number of persons suffering from dementia by targeting atherosclerosis.ID:A2017424FCollaborators:M. Arfan Ikram, MD, PhDMentors:Meike Vernooj, MD, PhDJuly 1, 2017 to June 30, 2019Alzheimer'sPostdoctoral Fellowship$98,823
- Esther G. Gonzalez, PhDKrembil Research Institute (Toronto, Canada)
Glaucoma is known as the “silent killer of vision” because a large proportion of people are not aware they have it until the late stages of the disease, and therefore it is very important to detect the disease early so these patients get help. It is also important to understand the disease in order to develop new lines of treatments. There are new indications that changes occur not only in the eyes but also in the brain of these patients, particularly in a structure that connects the two brain hemispheres. We plan to study the function of this brain structure in humans with glaucoma using a series of non-invasive tests.
This grant was transferred to Dr. Esther G. Gonzalez upon the passing of the original PI, Dr. Martin Steinbach in June 2017. The research project is being continued in Martin's memory.ID:G2017093July 1, 2017 to June 30, 2019GlaucomaStandard$150,000
- Ji Yi, PhDBoston Medical Center (Boston, MA)
Glaucoma is an eye disease that affects millions of American’s vision. The best way to slow and stop the disease is to detect it early; however, existing methods are insufficient to do so. We plan to develop a new optical imaging technology to examine the eye, which is very sensitive to early glaucoma so that we can use it for early diagnosis. This project not only may benefit many people by helping to prevent blindness, but also could enhance our understanding how this disease develops.ID:G2017077Collaborators:Manishi Desai, MDJuly 1, 2017 to June 30, 2019GlaucomaStandard$150,000
- Pietro Michelucci, PhDHuman Computation Institute (Ithaca, NY)
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.ID:CA2017606July 1, 2017 to June 30, 2019Alzheimer'sOther$484,910
- Sarah McFarlane, PhDUniversity of Calgary (Canada)
In neovascular age-related macular degeneration (AMD), the sprouting of new blood vessels (angiogenesis/neovascularization) leads to the death of the nerve cells of the retina. Neovascular AMD places a substantial burden on patients and the healthcare system. Current approaches to block new blood vessels from forming are not effective in many patients and they have serious side effects. There’s an urgent need for effective new ways to prevent these faulty new blood vessels from forming, but not affect the health of retinal nerve cells or the normal blood vessels. To address this need, we are developing a genetic animal model where we can rapidly identify novel, safe and effective drugs for the treatment of neovascular AMD.ID:M2017002July 1, 2017 to June 30, 2019Macular DegenerationStandard$123,160
- Ephraim F. Trakhtenberg, PhDUniversity of Connecticut Health Center (Farmington, CT)
The biological molecular mechanisms controlling the growth of connections in the central nervous system (CNS) are still poorly understood. The inability of the eye to regenerate such connections to the brain is the key reason why vision is lost from optic nerve damage, which can happen in a disease such as glaucoma, cannot be restored. We propose to identify novel biological regulators of the intrinsic ability of the retinal cells to regrow such connections between the eye and the brain. These studies could lead to the development of therapeutics for restoring simple visual abilities to those who became blind due to angle-closure glaucoma, and possibly other types of glaucoma.ID:G2017204July 1, 2017 to June 30, 2019GlaucomaStandard$150,000
- Derek Welsbie, MD, PhDUniversity of California, San Diego (La Jolla, CA)
Nerve cells called retinal ganglion cells (RGCs) form the connection between the eye and the brain. In glaucoma, these nerve cells die and vision is permanently lost. We have previously shown that a protein called dual leucine zipper kinase (DLK) is critical for the death of these cells. Thus, this proposal seeks to develop a gene therapy vector that might interfere with DLK and prevent RGC death and accompanying vision loss.ID:G2017212Collaborators:Donald J. Zack, MD, PhDJuly 1, 2017 to June 30, 2019GlaucomaStandard$150,000
Recipient of the Dr. Douglas H. Johnson Award
- Pierre De Rossi, PhDUniversity of Chicago (Chicago, IL)
Genetic studies have recently uncovered several genes that can elevate the risk of developing Alzheimer’s disease (AD), including the BIN1 gene as the second strongest genetic risk factor for late onset AD. My lab has generated a BIN1 transgenic model to mimic the increase of BIN1 protein in the brains of people with AD. My goal is to use this transgenic mouse model to investigate how BIN1 functions as a risk factor in AD. I expect that my proposed research will significantly advance the knowledge about BIN1's function in the physiology of the brain, and reveal how it contributes to AD pathology.ID:A2017366FMentors:Gopal Thinakaran, PhDJuly 1, 2017 to June 30, 2019Alzheimer'sPostdoctoral Fellowship$100,000
- Krishnakumar Kizhatil, PhDThe Jackson Laboratory (Bar Harbor, ME)
Glaucoma is a devastating neurodegenerative disease that causes blindness. Glaucoma results from increased pressure in the eye; however, the mechanistic basis of the pressure increase is largely undetermined. Neurons innervating the eye play a role in controlling pressure, but again the specific mechanisms are not clear. We will determine the mechanistic basis of neuronal control of eye pressure using mice and modern imaging and molecular methods.ID:G2017152Collaborators:Simon W. M. John, PhDJuly 1, 2017 to June 30, 2019GlaucomaStandard$150,000