Diet plays an important role in the development of many chronic diseases. However, we still don’t have a good understanding of which dietary components are most important for the prevention of Alzheimer’s disease (AD). In this project, we will identify key healthy dietary patterns that can form the foundation of dietary recommendations to lower Alzheimer’s risk. This is important because diet is among the risk factors that are modifiable; thus we can change our behavior and lower our risk of this devastating disease.
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- Majken Jensen, PhDHarvard University (Boston, MA)ID:A2017290SJuly 1, 2017 to June 30, 2020Alzheimer's DiseaseStandard$297,818
- Randy McIntosh, PhDBaycrest Centre for Geriatric Care (Toronto, Canada)
The brain is a complicated system whose different parts interact to support a variety of cognitive functions. This complexity makes it difficult to treat diseases such as Alzheimer’s and Parkinson’s, where many different brain areas can be affected, but lead to very similar deficits, such as memory dysfunction. Our research provides a framework of tools to “reconstruct” the brain and build models of different dementias to characterize the unique features of each disease and the final common paths to cognitive impairment. As our work progresses, it will be used to evaluate the potential of therapeutic interventions to help identify treatment targets, or areas of the brain that, if treated, are most likely to result in the best outcome for the individual.ID:A2017286SCo-principal Investigators:Kelly Shen, PhDCollaborators:Michael Breakspear, PhD; Viktor Jirsa, PhD; Petra Ritter, PhD; Ana Solodkin, PhDJuly 1, 2017 to June 30, 2020Alzheimer's DiseaseStandard$299,565
- Resham Chhabra, PhDJohns Hopkins University (Baltimore, MD)
My research aims to determine whether depletion of TAR DNA-binding protein 43 (TDP-43) in neurons contributes to pathological conversion of tau or accelerates tauopathy, a critical driver of neuron loss and cognitive decline in sporadic Alzheimer’s disease (AD). The pathological alteration and aggregation of tau protein (called tauopathy) is arguably the most important alteration in AD, as it shows the strongest association with the loss of brain cells and memory. Many studies have shown TDP-43 abnormality in 30-70% of AD cases, and that these cases show worsened memory loss. The aim of our study is to find out if TDP-43 loss plays a role in the initiation or acceleration of tauopathy in AD. Once we know what drives the changes in tau, we can halt or slow the progression of this disease.ID:A2017102FMentors:Tong Li, PhD; Philip Wong, PhDJuly 1, 2017 to June 30, 2019Alzheimer's DiseasePostdoctoral Fellowship$100,000
- Trevor McGill, PhDOregon Health and Science University (Portland, OR)
Age-related macular degeneration (AMD) is the most common cause of legal blindness in the elderly in developed countries, and is a leading cause of blindness worldwide. The typical American diet is low in nutritional factors that may reduce the risk or severity of AMD. The goal of this project is to determine whether being deprived of these nutrients has consequences for the development of AMD, and to determine the mechanisms by which this occurs. Results from these studies will provide direct evidence for the importance of these nutritional factors in maintaining retinal health and preventing advanced retinal disease, and may reveal new options for therapeutic intervention.ID:M2017073Collaborators:Paul S. Bernstein, MD, PhD; Martha Neuringer, PhDJuly 1, 2017 to June 30, 2019Macular DegenerationStandard$160,000
Recipient of The Carolyn K. McGillvray Award for Macular Degeneration Research
- Patsy Nishina, PhDThe Jackson Laboratory (Bar Harbor, ME)
Genes are made up of precise building blocks; imagine square blocks stacked together in an orderly fashion. Sometimes there are differences in these building blocks between people which may cause disease; for example, a building block may be shaped liked a triangle rather than a square, causing the stack to be unstable. In other instances, genetic variations may be benign, such as a color change from red to orange. Our goal is to determine which genetic variations are disease-causing and then to take that variant and create a mouse model that carries the disease-causing change. This mouse model could be used to study what the change in the building block does to the eye, how it leads to disease, and it can also be used to test different treatments.ID:M2017042Co-principal Investigators:Martin Pera, PhDJuly 1, 2017 to June 30, 2019Macular DegenerationStandard$160,000
- Inma Cobos, MD, PhDUniversity of California, Los Angeles, Ronald Reagan Medical Center (Los Angeles, CA) David Geffen School of Medicine at UCLA (Los Angeles, CA)
A close look at brain tissue from Alzheimer’s disease (AD) patients reveals that only some types of neurons have tau neurofibrillary tangles or others signs of neurodegeneration, while others in close vicinity appear healthy. What makes some neurons more vulnerable or resistant to disease? We are using a new technique, called single cell RNA sequencing, to isolate thousands of single neurons from human brain tissue, study all the genes that are expressed in each individual cell, and make cell-to-cell comparisons between normal, early stage and late stage AD. Our studies will clarify the precise identity of neurons involved by pathology and undergoing cell death in AD, and point to the main molecular pathways that confer vulnerability or resistance to disease.ID:A2017346SCollaborators:Giovanni Coppola, MD; Weizhe Hong, PhDJuly 1, 2017 to June 30, 2020Alzheimer's DiseaseStandard$300,000
This grant is made possible in part by support from Alzheimer’s Los Angeles.
- Chaeyoung Kim, PhDGladstone Institutes (San Francisco, CA)
Apolipoprotein E (apoE) has important roles in both normal central nervous system physiology and neuropathology, such as Alzheimer’s disease (AD). Importantly, the apoE4, one of apoE isoforms, is the major genetic risk factor for AD, and generates toxic fragments that cause mitochondrial dysfunction and drive neurodegeneration. Because mitochondrial dysfunction and metabolic impairment are critical elements of AD pathology, I will study how apoE4 and its neurotoxic fragments interact with mitochondria and alter mitochondrial activity. This largely unexplored approach will provide insight into the mechanisms underlying the role of apoE4 in AD and may identify new therapeutic targets to treat apoE4-associated AD.ID:A2017214FMentors:Robert W. Mahley, MD, PhDJuly 1, 2017 to June 30, 2019Alzheimer's DiseasePostdoctoral Fellowship$100,000
- 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
- Tao Ma, MD, PhDWake Forest University School of Medicine (Winston-Salem, NC)
The basic causes underlying the cognitive deterioration in Alzheimer’s disease (AD) and other dementias remain elusive, which hampers the development of any effective therapies. This project will shed light on whether new proteins synthesized in association with a cellular signaling factor (eEF2K/eEF2 signaling) play a role in AD pathogenesis This work could inform future identification of novel diagnostic markers and therapeutic targets for AD and related cognitive syndromes.ID:A2017457SCollaborators:Christina M. Furdui, PhDJuly 1, 2017 to June 30, 2020Alzheimer's DiseaseStandard$300,000
- Philippe Mourrain, PhDStanford University (Stanford, CA)
Age-related macular degeneration (AMD) is one of the leading causes of blindness in the world but its genetics is still unclear. Most of the DNA variations in AMD patients are found outside of the genes, and it is extremely hard to know whether these variants are actual mutations and what genes they affect. We have found that some of these variants are located in genome regions conserved down to the zebrafish, and surrounded by the same neighborhood of genes as in the human genome. Their preservation in the zebrafish allows us to visualize in this transparent genetic vertebrate model whether these variants are just neutral or if they disrupt the regulation of one the neighbor genes, possibly revealing the actual gene affected in AMD human patients.ID:M2017209Co-principal Investigators:Romain Madelaine, PhDCollaborators:Jeffrey Goldberg, MD, PhD; Douglas Vollrath, MD, PhDJuly 1, 2017 to June 30, 2019Macular DegenerationStandard$160,000
This grant is made possible by support from the Nancy Ferguson Seeley Trust in memory of Mildred F. Ferguson.