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Genomes and Genes | Karen E DuffSummaryAffiliation: Columbia University Country: USA Publications
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Publications
Imaging brain amyloid of Alzheimer disease in vivo in transgenic mice with an Abeta peptide radiopharmaceuticalHwa Jeong Lee
Department of Medicine, UCLA School of Medicine, Los Angeles, California 90024, USA
J Cereb Blood Flow Metab 22:223-31. 2002..In conclusion, the results show that it is possible to image the Abeta amyloid burden in the brain in vivo with an amyloid imaging agent, provided the molecule is conjugated to a blood-brain barrier drug-targeting system...- Transgenic mouse models of Alzheimer's disease: how useful have they been for therapeutic development?Karen Duff
Nathan Kline Institute, Department of Psychiatry, New York University, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA
Brief Funct Genomic Proteomic 3:47-59. 2004.... - Normal and abnormal tau neurobiologyKaren Duff
Taub Institute, Columbia University, New York State Psychiatric Institute, 650 W168th St, New York, NY 10032, USA
Alzheimer Dis Assoc Disord 20:202-5. 2006 - Phenothiazine-mediated rescue of cognition in tau transgenic mice requires neuroprotection and reduced soluble tau burdenJohn C O'Leary
Department of Molecular Medicine, Byrd Alzheimer s Research Institute, University of South Florida, Tampa, FL 33613, USA
Mol Neurodegener 5:45. 2010..Thus, efforts to discover therapeutics for tauopathies emphasize soluble tau reductions as well as neuroprotection... - Disaggregation of tau as a therapeutic approach to tauopathiesK Duff
Taub Institute Department of Pathology, Columbia University and Dept of Integrative Neuroscience, New York State Psychiatric Institute, New York, USA
Curr Alzheimer Res 7:235-40. 2010..In addition, this effect is achieved without altering levels of phosphorylation at disease and microtubule binding relevant epitopes... - Anesthesia-induced hyperphosphorylation detaches 3-repeat tau from microtubules without affecting their stability in vivoEmmanuel Planel
Taub Institute for Alzheimer s Disease Research, Department of Pathology, Columbia University Medical Center, New York, New York 10032, USA
J Neurosci 28:12798-807. 2008..Tau remaining on the MTs under these conditions is sufficient to maintain MT network integrity... - Inhibition of tau polymerization with a cyanine dye in two distinct model systemsErin E Congdon
Department of Pathology, Taub Institute, Columbia University and Department of Integrative Neuroscience, New York State Psychiatric Institute, New York, New York 10032, USA
J Biol Chem 284:20830-9. 2009..Overall, a cyanine dye can dissociate aggregated Tau in an ex vivo model of tauopathy with little toxicity and exploration of the use of these type of dyes as therapeutic agents is warranted... - Phospholipase d2 ablation ameliorates Alzheimer's disease-linked synaptic dysfunction and cognitive deficitsTiago Gil Oliveira
Department of Pathology and Cell Biology, Taub Institute for Research on Alzheimer s Disease and the Aging Brain, Columbia University Medical Center, New York, New York 10032, USA
J Neurosci 30:16419-28. 2010..Collectively, our results point to specific molecular species of PA as key modulators of AD pathogenesis and identify PLD2 as a novel potential target for therapeutics... - Linking Abeta and tau in late-onset Alzheimer's disease: a dual pathway hypothesisScott A Small
Taub Institute for Research on Alzheimer s Disease and the Aging Brain, Department of Neurology, Columbia University College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
Neuron 60:534-42. 2008..This model may account for the results of recent drug trials and, if confirmed, may guide future drug development... - Is tau aggregation toxic or protective?Erin E Congdon
Taub Institute for Research on Alzheimer s Disease, Department of Pathology, Columbia University, New York, NY, USA
J Alzheimers Dis 14:453-7. 2008..Indeed, if monomeric or oligomeric species are mediators of disease, formation of larger tau filaments may prove beneficial to affected cells. This review will examine the findings regarding the toxicity of various tau species... - Hyperphosphorylation and aggregation of tau in mice expressing normal human tau isoformsCathy Andorfer
Departments of Neuroscience and Pathology, Albert Einstein College of Medicine, Bronx, New York, USA
J Neurochem 86:582-90. 2003..This pathologic tau accumulates in the cell bodies and dendrites of neurons in a spatiotemporally relevant distribution... - Detection of Alzheimer's amyloid in transgenic mice using magnetic resonance microimagingYoussef Zaim Wadghiri
Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, New York 10016, USA
Magn Reson Med 50:293-302. 2003..This approach provides an in vivo method to detect Abeta in AD transgenic mice, and suggests that diagnostic MRI methods to detect Abeta in AD patients may ultimately be feasible... - Presenilins are enriched in endoplasmic reticulum membranes associated with mitochondriaEstela Area-Gomez
Department of Neurology, Columbia University Medical Center, New York, New York, USA
Am J Pathol 175:1810-6. 2009.... - Amyloid-beta deposition is associated with decreased hippocampal glucose metabolism and spatial memory impairment in APP/PS1 miceMarcin Sadowski
Department of Neurology, New York University School of Medicine, New York, New York 10016, USA
J Neuropathol Exp Neurol 63:418-28. 2004..5% +/- 0.4% at 8 months to 17.4% +/- 4.6%. These findings implicate Abeta or APP in the behavioral and metabolic impairments in APP/PS1 mice and the failure to compensate functionally for PS1-related hippocampal cell loss... - Interplay between cyclin-dependent kinase 5 and glycogen synthase kinase 3 beta mediated by neuregulin signaling leads to differential effects on tau phosphorylation and amyloid precursor protein processingYi Wen
Taub Institute at Columbia University Medical Center, New York State Psychiatric Institute, New York, New York 10032, USA
J Neurosci 28:2624-32. 2008..Thus, cdk5 inhibitors may not be effective in targeting tau phosphorylation in the elderly... - Retromer deficiency observed in Alzheimer's disease causes hippocampal dysfunction, neurodegeneration, and Abeta accumulationAlim Muhammad
Taub Institute for Research on Alzheimer s Disease and the Aging Brain, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA
Proc Natl Acad Sci U S A 105:7327-32. 2008..By recapitulating features of the disease, these animal models suggest that retromer deficiency observed in late-onset Alzheimer's disease can contribute to disease pathogenesis... - A transgenic rat that develops Alzheimer's disease-like amyloid pathology, deficits in synaptic plasticity and cognitive impairmentLi Liu
Department of Pathology, Taub Institute for Research on Alzheimer s Disease, Columbia University, Black Building 5 513, 650 West 168th Street, New York, NY 10032, USA
Neurobiol Dis 31:46-57. 2008.... - Fibrillar amyloid deposition leads to local synaptic abnormalities and breakage of neuronal branchesJulia Tsai
Molecular Neurobiology Program, Skirball Institute and Department of Neuroscience and Physiology, New York University School of Medicine, New York, New York 10016, USA
Nat Neurosci 7:1181-3. 2004..Thus, fibrillar amyloid deposition is more detrimental to neuronal circuitry than previously thought, underscoring the importance of prevention and early clearance of plaques... - Links between the pathology of Alzheimer's disease and vascular dementiaMarcin Sadowski
Department of Neurology, New York University School of Medicine, New York, New York 10016, USA
Neurochem Res 29:1257-66. 2004..In this paper, we review some of the links between vascular risk factors and AD pathology and present data on the direct effect of ischemia on cognitive function and A beta deposition in a mouse model of AD... - Transcriptional regulation of beta-secretase by p25/cdk5 leads to enhanced amyloidogenic processingYi Wen
Taub Institute at Columbia University Medical Center, New York, NY 10032, USA
Neuron 57:680-90. 2008..These data demonstrate a pathway by which p25/cdk5 increases the amyloidogenic processing of APP through STAT3-mediated transcriptional control of BACE1 that could have implications for AD pathogenesis... - Lowering beta-amyloid levels rescues learning and memory in a Down syndrome mouse modelWilliam J Netzer
Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, New York, USA
PLoS ONE 5:e10943. 2010..This treatment corrected learning deficits characteristic of these mice, suggesting that beta-amyloid-lowering therapies might improve cognitive function in young DS patients... - Collapsin response mediator protein-2 hyperphosphorylation is an early event in Alzheimer's disease progressionAdam R Cole
Division of Pathology and Neurosciences, University of Dundee, Ninewells Hospital, Dundee, Scotland, UK
J Neurochem 103:1132-44. 2007..These observations implicate hyperphosphorylation of CRMP2 as an early event in the development of AD and suggest that it can be induced by a severe APP over-expression and/or processing defect... - Changes in apolipoprotein E expression in response to dietary and pharmacological modulation of cholesterolSuzana S Petanceska
Center for Dementia Research, Nathan Kline Institute, Orangeburg NY 10962, USA
J Mol Neurosci 20:395-406. 2003..These observations suggest that disrupted cholesterol metabolism may increase the risk of developing AD in part due to the effect of cholesterol on brain ApoE expression... - Histological co-localization of iron in Abeta plaques of PS/APP transgenic miceMaria F Falangola
Center for Advanced Brain Imaging, Nathan Kline Institute for Psychiatric Research, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA
Neurochem Res 30:201-5. 2005.... - Antibody against C-terminal Abeta selectively elevates plasma AbetaAudrey J Gray
Department of Neurology, Georgetown University Medical Center, Washington, DC 20057, USA
Neuroreport 18:293-6. 2007..In this study, we found that anti-amyloid beta 40-specific antibody induces amyloid beta sequestration. These results indicate that C-terminal antibodies may be useful in amyloid beta sequestration therapy... - Visualization of beta-amyloid plaques in a transgenic mouse model of Alzheimer's disease using MR microscopy without contrast reagentsSang Pil Lee
Center for Advanced Brain Imaging, The Nathan Kline Institute, Orangeburg, NY 10962, USA
Magn Reson Med 52:538-44. 2004..Furthermore, the detection of beta-amyloid plaques was achieved with a scan time as short as 2 hr, approaching the scan time considered reasonable for in vivo imaging... - Statin therapy for Alzheimer's disease: will it work?Suzana S Petanceska
Nathan S Kline Institute for Psychiatric Research, Dementia Research Group, Orangeburg, NY, 10962, USA
J Mol Neurosci 19:155-61. 2002..Our results indicate that Lipitor treatment markedly attenuates A beta deposition in this animal model... - Organotypic slice cultures from transgenic mice as disease model systemsKaren Duff
Nathan Kline Institute and Department of Psychiatry, New York University, 140 Old Orangeburg Rd, Orangeburg, NY 10962, USA
J Mol Neurosci 19:317-20. 2002..Organotypic slice models are currently being used to test the impact of tangle enhancers or inhibitors as a prescreen for efficacy before testing drugs in vivo... - MRI assessment of neuropathology in a transgenic mouse model of Alzheimer's diseaseJoseph A Helpern
Nathan S Kline Institute, Orangeburg, New York 10962, USA
Magn Reson Med 51:794-8. 2004..No differences in T(1) values or proton density were detected between any groups of mice. These results indicate that T(2) may be a sensitive marker of abnormalities in this transgenic mouse model of AD... - Mostly separate distributions of CLAC- versus Abeta40- or thioflavin S-reactivities in senile plaques reveal two distinct subpopulations of beta-amyloid depositsHisatomo Kowa
Department of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, University of Tokyo, 7 3 1 Bunkyo ku, Hongo, Tokyo 113 0033, Japan
Am J Pathol 165:273-81. 2004.... - Cholesterol in Alzheimer's disease and tauopathyMark Burns
Center for Dementia Research, Nathan S. Kline Institute, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA
Ann N Y Acad Sci 977:367-75. 2002.... - Brain damage results in down-regulation of N-acetylaspartate as a neuronal osmolyteMorris H Baslow
Nathan S Kline Institute for Psychiatric Research, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA
Neuromolecular Med 3:95-104. 2003..The NAA system, when present in the brain, appears to reflect a high degree of cellular integration, and therefore may be a unique metabolic construct of the intact vertebrate brain... - Presenilin redistribution associated with aberrant cholesterol transport enhances beta-amyloid production in vivoMark Burns
Center for Dementia Research, Nathan S Kline Institute, Orangeburg, New York 10962, USA
J Neurosci 23:5645-9. 2003..Our results show that aberrant cholesterol trafficking is associated with the potentiation of APP processing components in vivo, leading to an overall increase in Abeta levels... - Cdk5 is a key factor in tau aggregation and tangle formation in vivoWendy Noble
Center for Dementia Research, Nathan S Kline Institute, New York University, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA
Neuron 38:555-65. 2003..Insoluble tau was also associated with active GSK. Thus, cdk5 can initiate a major impact on tau pathology progression that probably involves several kinases. Kinase inhibitors may thus be beneficial therapeutically... - Use of in vivo models to study the role of cholesterol in the etiology of Alzheimer's diseaseMark Burns
Center for Dementia Research, Nathan S Kline Institute, Orangeburg, New York 10962, USA
Neurochem Res 28:979-86. 2003..Data from in vivo and in vitro studies will then be presented to describe how treatments aimed at modulating lipid levels may be efficacious in treating AD... - Inhibition of glycogen synthase kinase-3 by lithium correlates with reduced tauopathy and degeneration in vivoWendy Noble
Center for Dementia Research, Nathan S Kline Institute, New York University, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA
Proc Natl Acad Sci U S A 102:6990-5. 2005..These results support the idea that kinases are involved in tauopathy progression and that kinase inhibitors may be effective therapeutically... - Co-localization of cholesterol, apolipoprotein E and fibrillar Abeta in amyloid plaquesMark P Burns
Center for Dementia Research, Nathan S Kline Institute, 140 Old Orangeburg Rd, Orangeburg, NY 10962, USA
Brain Res Mol Brain Res 110:119-25. 2003.... - Presenilin mutations in familial Alzheimer disease and transgenic mouse models accelerate neuronal lysosomal pathologyAnne M Cataldo
Laboratory for Molecular Neuropathology, Mailman Research Center, McLean Hospital, Belmont, Massachusetts, USA
J Neuropathol Exp Neurol 63:821-30. 2004..Our findings suggest that presenilin mutations have amyloid-independent effects on the lysosomal system, which are synergistic with the lysosomal system pathology that is associated with beta-amyloid... - Novel therapeutic approach for the treatment of Alzheimer's disease by peripheral administration of agents with an affinity to beta-amyloidYasuji Matsuoka
The Center for Dementia Research, Nathan Kline Institute, Orangeburg, New York 10962, USA
J Neurosci 23:29-33. 2003.... - Cell-cycle reentry and cell death in transgenic mice expressing nonmutant human tau isoformsCathy Andorfer
Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461, USA
J Neurosci 25:5446-54. 2005.... - Rapid neurofibrillary tangle formation after localized gene transfer of mutated tauRonald L Klein
Department of Pharmacology and Therapeutics, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130, USA
Am J Pathol 164:347-53. 2004..The ability to produce neurofibrillary pathology in adult rodents makes this a useful method to study tau-related neurodegeneration... - Axonal transport rates in vivo are unaffected by tau deletion or overexpression in miceAidong Yuan
Center for Dementia Research, Nathan Kline Institute, Orangeburg, New York 10962, USA
J Neurosci 28:1682-7. 2008..These results suggest that tau is not essential for axonal transport and that transport rates in vivo are not significantly affected by substantial fluctuations in tau expression... - Untangling memory deficitsKaren Duff
Nat Med 11:826-7. 2005 - Macroautophagy--a novel Beta-amyloid peptide-generating pathway activated in Alzheimer's diseaseW Haung Yu
Center for Dementia Research, Nathan Kline Institute, Orangeburg, NY 10962, USA
J Cell Biol 171:87-98. 2005..Our results, therefore, link beta-amyloidogenic and cell survival pathways through macroautophagy, which is activated and is abnormal in AD... - The amyloid pathology progresses in a neurotransmitter-specific mannerKaren F S Bell
Department of Pharmacology and Therapeutics, McGill University, 3655 Sir William Osler Promenade, Montreal, Que, Canada, H3G 1Y6
Neurobiol Aging 27:1644-57. 2006..Subsequent staining in AD brain tissue revealed the novel presence of glutamatergic dystrophic neurites, to our knowledge the first evidence of a structural glutamatergic deficit in the AD pathology... - Using proteomics and network analysis to elucidate the consequences of synaptic protein oxidation in a PS1 + AbetaPP mouse model of Alzheimer's diseaseBrian A Soreghan
Department of Pharmaceutical Sciences, University of Southern California, Los Angeles, CA 90033, USA
J Alzheimers Dis 8:227-41. 2005..We believe the results of these studies will help establish an initial AD database of oxidatively modified proteins and provide a foundation for the design of future hypothesis driven research in the areas of aging and neurodegeneration... - The effects of ABCA1 on cholesterol efflux and Abeta levels in vitro and in vivoMark P Burns
Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20007, USA
J Neurochem 98:792-800. 2006..These data show that promoting cholesterol efflux is a viable target for Abeta reducing strategies; however, knockout of cholesterol transporters is not sufficient to alter Abeta in vitro or in vivo... - Cholesterol distribution, not total levels, correlate with altered amyloid precursor protein processing in statin-treated miceMark P Burns
Center for Dementia Research, Nathan S Kline Institute New York University, Orangeburg, NY 10962, USA
Neuromolecular Med 8:319-28. 2006..This data suggests that cholesterol distribution and not total cholesterol levels may be important to Abeta production in the CNS... - Rat transgenic models with a phenotype of intracellular Abeta accumulation in hippocampus and cortexValentina Echeverria
Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada
J Alzheimers Dis 6:209-19. 2004..A preliminary protein analysis of the hippocampus of the double transgenic rat (UKUR25) by mass spectrometry showed differences in the protein profile between this transgenic line and controls... - Development of Abeta terminal end-specific antibodies and sensitive ELISA for Abeta variantYuko Horikoshi
Immuno-Biological Laboratories Co, Ltd, Fujioka-Shi, Gunma 375-0005, Japan
Biochem Biophys Res Commun 319:733-7. 2004..A combination of C-termini antibodies and an antibody against the middle region of Abeta detects mouse Abeta in non-transgenic mouse brains... - An Abeta sequestration approach using non-antibody Abeta binding agentsYasuji Matsuoka
Department of Neurology, Georgetown University Medical Center, Washington, DC 20057, USA
Curr Alzheimer Res 2:265-8. 2005..Unfortunately, peripheral administration for three weeks did not substantially alter brain Abeta load. Optimized Abeta binding agents with high affinity to soluble Abeta are necessary for the sequestration approach... - Dense-core plaques in Tg2576 and PSAPP mouse models of Alzheimer's disease are centered on vessel wallsSamir Kumar-Singh
Department of Molecular Genetics VIB8, Neurodegenerative Brain Diseases Research Group, Molecular Neuropathology Project, University of Antwerp, Universiteitsplein 1, B 2610 Antwerp, Belgium
Am J Pathol 167:527-43. 2005....