Funded Research
(listed chronologically)
| Project Description | Researchers | Funding |
|---|---|---|
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Cellular and Animal Models of Amyloid Pathology in Early Alzheimer's Disease The goal of this project is to evaluate the pathological significance of a new type of Abeta deposits in the brain (at the onset of Alzheimer’s disease) in order to develop a novel mechanism for amyloid pathogenesis to help convince the FDA to approve and support early clinical trials. |
Charles Glabe, Ph.D. |
2011 $100,000 |
|
Effect of Bexarotene on Abeta in APP Tg Mice Expressing ApoE3 and ApoE4 The goal of this project is to determine the effects of bexarotene on both Abeta and ApoE metabolism in the presence of human Abeta and human ApoE isoforms (any of two or more functionally similar proteins that have a similar but different amino acid sequence) because it is relevant to potential effects of similar drugs in humans. |
2011 $100,000 |
|
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Exploring Adult Neurogenesis as a Therapeutic Target for Alzheimer's Disease The goal of this project is to test whether the strategy of stimulating endogenous stem cells in the AD brain is safe in order to find treatment for Alzheimer’s patients. Recent evidence shows the adult brain contains discrete populations of stem cells that retain the capacity to generate new neurons through the process of neurogenesis. Dr. Se Hoon Choi will test whether the strategy of stimulating endogenous stem cells in the AD brain is safe and effective ultimately to find treatment for Alzheimer’s patients. |
Se Hoon Choi, Ph.D. |
2011 $100,000 |
|
Mechanisms of Retinoid X Receptor-Mediated Abeta Clearance in Alzheimers' Disease The goal of this project is to investigate the mechanisms through which RXRs (retinoid x nuclear receptor) promote amyloid clearance from the brain. |
2011 $100,000 |
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Metallomic Mapping of the Aging Brain in Trg2576 Transgenic Mouse Model The goal of this project is to perform the first high-resolution metallomic brain maps of key biometals (copper, zinc, iron) during normal brain aging and in Alzheimer’s disease in order to develop disease-modifying treatments that target normalization of biometal distribution and metal-protein interactions in the brain. |
Lee Goldstein, MD, Ph.D. |
2011 $100,000 |
|
Modulation of Abeta Deposition by Cell-Specific Mechanisms The goal of this project is to determine which types of cells and factors in the brain influence excess Abeta deposition in Alzheimer’s patients, using animal models of the disease. |
Sangram S. Sisodia, Ph.D. |
2010 - 2011 $100,000 |
|
Molecular Tweezers—Novel Inhibitors of Amyloidogenic Proteins and Promising Drug Candidates for Alzheimer’s Disease The goal of this project is to plan expanded in vivo characterization of the efficacy of “molecular tweezers” toward development of disease-modifying therapy for AD and related diseases. |
Gal Bitan, Ph.D. |
2011 $100,000 |
|
Passive Tau Immunology Neurofibrillary tangles (NFTs) are biomarkers for Alzheimer’s disease and are the products of a breakdown in part of the structure of cells (Tau), leading to neural cell death. The goal of this project is to establish the first cellular system that develops authentic NFT-like Tau aggregates to provide mechanistic insights into NFT pathogenesis and a potential tool for identifying Tau- based therapeutics. |
Virginia M.-Y. Lee, Ph.D., M.B.A. |
2010 - 2011 $100,000 |
|
Selective Cell Vulnerability in Alzheimer's Disease The goal of this project is to identify cells that are both most vulnerable and most resistant to Alzheimer’s disease in order to develop drugs that will protect the most vulnerable. |
Paul Greengard, Ph.D. |
2011 $100,000 |
|
Structural and Functional Analysis of Novel Abeta and Tau Oligomers Using Conformation-Specific Monoclonal Antibodies The goal of this project is to determine which oligomers of Abeta and Tau are most damaging and whether specific antibodies can prevent formation of those oligomers. |
George S. Bloom, Ph.D. |
2011 $100,000 |
|
Understand the Role of ADAM10 in the Pathogenesis of Alzheimer's Disease After Head Trauma The goal of this project is to determine whether increased sAPPα levels are capable of reducing the production of neurotoxic Abeta following head trauma in order to reduce the risk of developing Alzheimer’s disease following brain injury. |
Giuseppina Tesco, MD, Ph.D. |
2011 $100,000 |
|
Understanding the Up-Regulation of Neuroserpin in the Alzheimer’s Brain and Isolating a Potential Therapeutic Inhibitor of its Action: Continued The goal of this project is to determine if there is a strong correlation between Alzheimer’s patients with high neuroserpin and high thyroid hormone levels (for both males and females). Since our initial proposal in Spring 2010, several papers have appeared making the association between thyroid hormone levels and dementia. Thyroid hormones are associated with poorer cognition in mild cognitive impairment. (Dementia Geriatrics & Cognitive Disorders 30:205-11. Bensenor, IM et al. 2010, Subclinical hyperthyroidism and dementia. BMC Public Health 10:298.) |
Nicholas Seeds, Ph.D. |
2010 - 2011 $100,000 |
|
Curcumin Collaborative Project This collaborative project will identify and characterize novel curcumin-like derivatives for the treatment and prevention of Alzheimer’s disease. The purpose of the study is to develop means of overcoming obstacles to rapid breakdown and creating methodologies for precisely delivering curcumin derivatives to appropriate locations within the brain. |
2010 $400,000 |
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Three Studies of ACAT Inhibitors as Potential Therapies for AD It is known that high cholesterol is associated with cardiovascular disease. Cholesterol also regulates the production of the toxic amyloid beta (Aβ) peptide in Alzheimer’s disease (AD). Therapies already developed or in development for dyslipidemia and atherosclerosis are becoming attractive for reducing Aβ in the brains of patients affected by AD. |
Dora M. Kovacs, Ph.D. |
2004 - 2010 $300,000 |
|
Novel Soluable Gamma-Secretase Modulators Building on in vitro characterization of a novel series of soluable gamma-secretase modulators (SGSMs) funded by Cure Alzheimer’s Fund, the current project is a thorough pharmacological or in vivo examination of these molecules to identify the best or “lead” drug candidate. |
2010 $250,000 |
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Anti-APOE Antibodies In this project, the researchers hypothesize that targeting apoE, a component of amyloid plaques, can result in less Aβ aggregation in the brain and decreased Aβ-related pathology and that this treatment will have fewer side effects than the use of anti-Aβ antibodies. The project will test this hypothesis in this proposal in the context of human apoE isoforms. |
David Michael Holtzman, MD |
2010 $100,000 |
|
NMDA Receptors The traditional signaling induced by NMDA-Rs is triggered by the Ca2+ ions that pass through the NMDA-R channel. However, preliminary data indicate that blockers at the NR2B subunit, but not the NR1 subunit or the channel of the NMDA receptor, prevent the synaptic effects of the NMDA receptor. These findings suggest that Abeta employs novel, non-ion flux NMDA-R signaling mechanisms to produce synaptic depression. These results may open up a new group of potential therapeutic targets for treatment of Alzheimer’s disease. |
Robert Malinow, MD, Ph.D. |
2010 $100,000 |
|
Mouse Model for Non-Generic Alzheimer's Disease The SAMP8 mouse model line is a model of accelerated senescence, and interestingly, develops sparse amyloid plaques, which is remarkable given the less amyloidogeneic properties of murine Aß. Hence, the research hypothesis for this project is that by introducing the more amyloidogenic human APP at the endogenous locus, researchers will be able to more robustly mimic the onset of sporadic Alzheimer’s disease, and thereby utilize this model for pre-clinical development and for widespread distribution to other investigators in the field. |
Frank La Ferla, Ph.D. |
2010 $63,851 |
|
Peek and Treat Approach to Diagnosis, Treatment and Monitoring of AD The objective of this project is to develop a nanotechnology platform that can simultaneously be used to diagnose and treat Alzheimer's. The work will explore how to develop multifunctional nanocarriers that contain both an imaging agent and a therpeutic agent and also will improve the binding capabilities of the nanocarrier allowing regulation of the release of therapeutic molecules to amyloid lesions. |
2010 $40,000 |
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Core Facility for Abeta Microdialysis Drug Discovery Platform In collaboration with an anonymous funder, Cure Alzheimer’s Fund is supporting development of a facility to measure the concentration of Amyloid-beta in real time in the brain of living, behaving mouse models that develop features of AD. The model enables screening for drugs that lower Amyloid-beta directly in the brain in relatively high throughput. |
David Michael Holtzman, MD |
2007 - 2009 $278,238 |
