Alzheimer's Disease Research - Current Awards Tae-Wan Kim, Ph.D.Columbia University Medical Center Title: Novel CNS Transporter Target in Alzheimer's Disease Summary: Dr. Tae-Wan Kim and colleagues have identified an ‘atypical monoamine transporter’ as a novel therapeutic target in Alzheimer's disease. The proposed research is designed to further validate the new target and generate therapeutic lead compounds. Further research will be conducted to understand this target in greater depth, using cell biological approaches. Program: Alzheimer's Disease  Soong Ho Kim, Ph.D.Mount Sinai School of Medicine Title: Testing of Group II mGluR Antagonist as a Potential AD Treatment Mentor:
Sam Gandy, M.D., Ph.D.
Mount Sinai School of Medicine (Mentor and Co-PI) Summary: Dr. Soong Ho Kim and colleagues are testing a drug candidate that may potentially reduce brain levels of amyloid beta protein, which has been shown to be toxic to brain cells. This drug has also been shown to enhance brain function, act as an anti-depressant and anti-anxiety medication, and have the potential to encourage the brain to replace damaged cells involved in learning and memory. Program: Alzheimer's Disease  Jungsu Kim, Ph.D.Washington University Title: Role of a LDLR-interacting protein in LDLR, ApoE, and Abeta Metabolism Summary: Genetic variants of the Apolipoprotein E (ApoE) gene represent the strongest genetic risk factor for Alzheimer's disease (AD). Dr. Jungsu Kim’s previous studies suggest that low density lipoprotein receptor (LDLR) binds to ApoE protein and dramatically affects the development of AD. In the current experiments, he is investigating the role of a novel LDLR-interacting protein in regulating LDLR and ApoE protein levels in order to test its potential as an AD therapeutic. Program: Alzheimer's Disease  Hwajin Kim, Ph.D.The J. David Gladstone Institutes Title: Mitochondrial Fission at the Synapse in Alzheimer’s Disease Mentor:
Ken Nakamura, M.D., Ph.D. (Primary Mentor), Lennart Mucke, M.D., (Co-Mentor)
Gladstone Institutes Summary: Mitochondria are vital organelles that generate energy. The fragmentation of mitochondria appears to play an important role in the pathogenesis of Alzheimer’s disease (AD). In this project, Dr. Hwajin Kim is studying the mechanisms by which mitochondrial fission may contribute to AD and is testing whether reversal of mitochondrial fission may be an effective therapeutic strategy for preventing AD progression. Program: Alzheimer's Disease  Bruce Lamb, Ph.D.Lerner Research Institute at Cleveland Clinic Title: Role of p38 MAPK in the Microglial-Mediated Alzheimer's Disease Tau Pathology Co-PI(s):
Kiran Bhaskar, Ph.D. ,
Summary: In a recent study (published in October 7th, 2010 issue of the journal NEURON), we have identified p38 MAPK as a link between neuroinflammation, cell-autonomous to microglia, and Alzheimer's disease tau pathology. In the current study, the role of a safe, orally bioavailable and brain permeable p38 MAPK inhibitor (MW01-2-069A-SRM) in preventing tau pathology will be examined both in vitro utilizing primary neurons and in vivo utilizing a unique transgenic mouse model of tauopathy (hTau mice). Program: Alzheimer's Disease  Gary Landreth, Ph.D.Case Western Reserve University Title: RXR: A Therapeutic Target in Neurodegenerative Disease Summary: A new rexinoid drug can rapidly remove existing plaques and lower Abeta peptide levels with improvement in memory and cognition within one week in amyloidogenic mouse models of AD. We propose to determine if this drug acts to prevent neuronal loss and dysfunction in two mouse models of neurodegeneration due to overproduction of Abeta or a mutant form of tau. Program: Alzheimer's Disease  Yueming Li, Ph.D.Sloan-Kettering Institute for Cancer Research Title: Effects of aging and gender on gamma-secretase Summary: The vast majority of Alzheimer's disease (AD) is sporadic in nature and has no known genetic basis. Aging and gender are common risk factors for the development of AD. This project will elucidate the role of aging and gender in the modulation of gamma-secretase that is linked with AD. Program: Alzheimer's Disease  Seth S. Margolis, Ph.D.Johns Hopkins University School of Medicine Title: Correcting Synapse Loss in the Alzheimer's Disease Brain Summary: Several recent studies, including those of Dr. Seth Shatkin Margolis and colleagues, suggest the intriguing hypothesis that neurodegenerative disorders such as Alzheimer's disease (AD) share a common causative feature, which is the loss of appropriate functional connections in the brain. Dr. Margolis’s team has identified a natural inhibitor of brain development and nerve cell connections that is increased in the AD brain. This project is aimed at discovering which symptoms of AD are due to the increased amount of this inhibitor and identifying small molecule blockers to this inhibitor as potential new treatments for AD. Program: Alzheimer's Disease  Sonia Mazzitelli, Ph.D.Harvard Medical School Title: Mechanism of RIP-1 in Mediating Abeta Neurotoxicity Mentor:
Junying Yuan, Ph.D.
Harvard Medical School Summary: Chronic inflammation is associated with a broad spectrum of neurodegenerative diseases of aging, including Alzheimer's disease (AD). Dr. Sonia Mazzitelli and colleagues propose a new way to investigate the connection between chronic inflammation and brain nerve-cell loss associated with AD. This research will provide relevant information to obtain a new target for a new type of therapy for AD. Program: Alzheimer's Disease  Masuo Ohno, Ph.D.Research Foundation for Mental Hygiene, Inc. at IBR Title: eIF2a Kinase GCN2 as a Target for Alzheimer's Therapy Summary: No treatment is currently available to slow or stop the deterioration of brain cells in Alzheimer's disease (AD), the most common cause of dementia in the elderly. The proposed study will test genetically engineered mouse models, which are expected to block the detrimental beta-secretase-elevating pathway and restore the memory-facilitating CREB function in AD. Our research has important implications for the development of a novel therapeutic approach to halt AD progression and improve synaptic and memory deficits associated with this devastating neurodegenerative disorder. Program: Alzheimer's Disease Last Review: 04/29/13 |
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