Efrat Levy

Summary

Affiliation: Nathan Kline Institute
Country: USA

Publications

  1. doi request reprint Cystatin C: a potential target for Alzheimer's treatment
    Efrat Levy
    Expert Rev Neurother 8:687-9. 2008
  2. pmc Induction of autophagy by cystatin C: a mechanism that protects murine primary cortical neurons and neuronal cell lines
    Belen Tizon
    Nathan S Kline Institute, Orangeburg, New York, United States of America
    PLoS ONE 5:e9819. 2010
  3. pmc The exosome secretory pathway transports amyloid precursor protein carboxyl-terminal fragments from the cell into the brain extracellular space
    Rocío Pérez-González
    Center for Dementia Research, Nathan S Kline Institute, Orangeburg, New York 10962, USA
    J Biol Chem 287:43108-15. 2012
  4. pmc Cystatin C in Alzheimer's disease
    Gurjinder Kaur
    Departments of Psychiatry, Biochemistry, and Molecular Pharmacology, Center for Dementia Research, Nathan S Kline Institute, New York University School of Medicine, Orangeburg NY, USA
    Front Mol Neurosci 5:79. 2012
  5. ncbi request reprint The role of cystatin C in cerebral amyloid angiopathy and stroke: cell biology and animal models
    Efrat Levy
    Department of Psychiatry, New York University School of Medicine, and Nathan Kline Institute, Orangeburg 10962, USA
    Brain Pathol 16:60-70. 2006
  6. ncbi request reprint Studies on the first described Alzheimer's disease amyloid beta mutant, the Dutch variant
    Efrat Levy
    Department of Pharmacology, New York University School of Medicine, New York, New York, USA
    J Alzheimers Dis 9:329-39. 2006
  7. ncbi request reprint Binding of cystatin C to Alzheimer's amyloid beta inhibits in vitro amyloid fibril formation
    Magdalena Sastre
    Departments of Pharmacology, New York University School of Medicine, 550 First Avenue, New York, NY, 10016, USA
    Neurobiol Aging 25:1033-43. 2004
  8. pmc Therapeutic effects of remediating autophagy failure in a mouse model of Alzheimer disease by enhancing lysosomal proteolysis
    Dun Sheng Yang
    Nathan Kline Institute, Orangeburg, NY, USA
    Autophagy 7:788-9. 2011
  9. ncbi request reprint Cystatin C inhibits amyloid-beta deposition in Alzheimer's disease mouse models
    Weiqian Mi
    Nathan S Kline Institute, Orangeburg, New York 10962, USA
    Nat Genet 39:1440-2. 2007
  10. pmc Immunization targeting a minor plaque constituent clears β-amyloid and rescues behavioral deficits in an Alzheimer's disease mouse model
    Jose Morales-Corraliza
    Center for Dementia Research, Nathan S Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USA
    Neurobiol Aging 34:137-45. 2013

Collaborators

Detail Information

Publications34

  1. doi request reprint Cystatin C: a potential target for Alzheimer's treatment
    Efrat Levy
    Expert Rev Neurother 8:687-9. 2008
  2. pmc Induction of autophagy by cystatin C: a mechanism that protects murine primary cortical neurons and neuronal cell lines
    Belen Tizon
    Nathan S Kline Institute, Orangeburg, New York, United States of America
    PLoS ONE 5:e9819. 2010
    ..Thus, modulation of CysC expression has therapeutic implications for stroke, Alzheimer's disease, and other neurodegenerative disorders...
  3. pmc The exosome secretory pathway transports amyloid precursor protein carboxyl-terminal fragments from the cell into the brain extracellular space
    Rocío Pérez-González
    Center for Dementia Research, Nathan S Kline Institute, Orangeburg, New York 10962, USA
    J Biol Chem 287:43108-15. 2012
    ....
  4. pmc Cystatin C in Alzheimer's disease
    Gurjinder Kaur
    Departments of Psychiatry, Biochemistry, and Molecular Pharmacology, Center for Dementia Research, Nathan S Kline Institute, New York University School of Medicine, Orangeburg NY, USA
    Front Mol Neurosci 5:79. 2012
    ..This review elaborates on the neuroprotective roles of CysC in AD and the clinical relevance of this protein as a therapeutic agent...
  5. ncbi request reprint The role of cystatin C in cerebral amyloid angiopathy and stroke: cell biology and animal models
    Efrat Levy
    Department of Psychiatry, New York University School of Medicine, and Nathan Kline Institute, Orangeburg 10962, USA
    Brain Pathol 16:60-70. 2006
    ..This review focuses on cell culture and animal models used to study the role of cystatin C in these processes...
  6. ncbi request reprint Studies on the first described Alzheimer's disease amyloid beta mutant, the Dutch variant
    Efrat Levy
    Department of Pharmacology, New York University School of Medicine, New York, New York, USA
    J Alzheimers Dis 9:329-39. 2006
    ..However, most AD patients have no genetic defects in AbetaPP, indicating that other factors may alter Abeta production, conformation, and/or clearance initiating the disease process...
  7. ncbi request reprint Binding of cystatin C to Alzheimer's amyloid beta inhibits in vitro amyloid fibril formation
    Magdalena Sastre
    Departments of Pharmacology, New York University School of Medicine, 550 First Avenue, New York, NY, 10016, USA
    Neurobiol Aging 25:1033-43. 2004
    ..Notably, cystatin C association with Abeta results in a concentration-dependent inhibition of Abeta fibril formation...
  8. pmc Therapeutic effects of remediating autophagy failure in a mouse model of Alzheimer disease by enhancing lysosomal proteolysis
    Dun Sheng Yang
    Nathan Kline Institute, Orangeburg, NY, USA
    Autophagy 7:788-9. 2011
    ..Our findings underscore the pathogenic significance of autophagic-lysosomal dysfunction in AD and demonstrate the value of reversing this dysfunction as an innovative therapeautic strategy for AD...
  9. ncbi request reprint Cystatin C inhibits amyloid-beta deposition in Alzheimer's disease mouse models
    Weiqian Mi
    Nathan S Kline Institute, Orangeburg, New York 10962, USA
    Nat Genet 39:1440-2. 2007
    ..Thus, cystatin C has a protective role in Alzheimer's disease pathogenesis, and modulation of cystatin C concentrations may have therapeutic implications for the disease...
  10. pmc Immunization targeting a minor plaque constituent clears β-amyloid and rescues behavioral deficits in an Alzheimer's disease mouse model
    Jose Morales-Corraliza
    Center for Dementia Research, Nathan S Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USA
    Neurobiol Aging 34:137-45. 2013
    ....
  11. doi request reprint In vitro assays measuring protection by proteins such as cystatin C of primary cortical neuronal and smooth muscle cells
    Sebastien A Gauthier
    Department of Psychiatry, New York University School of Medicine, New York, NY, USA
    Methods Mol Biol 849:275-87. 2012
    ..The effect of endogenous level of cystatin C expression is studied by comparing stressed primary cells isolated from brains of cystatin C transgenic, cystatin C knockout, and wild-type mice...
  12. pmc Cystatin C rescues degenerating neurons in a cystatin B-knockout mouse model of progressive myoclonus epilepsy
    Gurjinder Kaur
    Nathan S Kline Institute, 140 Old Orangeburg Rd, Orangeburg, NY 10962, USA
    Am J Pathol 177:2256-67. 2010
    ..Thus, CysC effectively rescues the CysB loss-of-function mutations, facilitating the reversal of pathophysiological changes and suggesting a novel therapeutic intervention for patients with EPM1 and other neurodegenerative disorders...
  13. pmc In vivo turnover of tau and APP metabolites in the brains of wild-type and Tg2576 mice: greater stability of sAPP in the beta-amyloid depositing mice
    Jose Morales-Corraliza
    Nathan Kline Institute for Psychiatric Research, Orangeburg, New York, USA
    PLoS ONE 4:e7134. 2009
    ..Given the neurotrophic roles attributed to sAPP, the enhanced stability of sAPP in the beta-amyloid depositing Tg2576 mice may represent a neuroprotective response...
  14. pmc Age-dependent dysregulation of brain amyloid precursor protein in the Ts65Dn Down syndrome mouse model
    Jennifer H K Choi
    Center for Dementia Research, Nathan Kline Institute, Orangeburg, New York 10962, USA
    J Neurochem 110:1818-27. 2009
    ..Therefore, multiple mechanisms contribute to the regulation towards diploid levels of APP metabolites in the Ts65Dn mouse brain...
  15. pmc Days to criterion as an indicator of toxicity associated with human Alzheimer amyloid-beta oligomers
    Sam Gandy
    Department of Neurology, Mount Sinai School of Medicine, New York, NY 10029, USA
    Ann Neurol 68:220-30. 2010
    ..We sought to study the bioactivities of endogenously formed oAbeta/ADDLs generated in situ from the physiological processing of human amyloid precursor protein (APP) and presenitin1 (PS1) transgenes...
  16. pmc Complexes of amyloid-beta and cystatin C in the human central nervous system
    Weiqian Mi
    Nathan S Kline Institute, Orangeburg, New York, USA
    J Alzheimers Dis 18:273-80. 2009
    ..Thus, enhancing CysC expression or modulating CysC binding to Abeta have important disease-modifying effects, suggesting a novel therapeutic intervention for AD...
  17. pmc Neuronal apoptosis and autophagy cross talk in aging PS/APP mice, a model of Alzheimer's disease
    Dun Sheng Yang
    Center for Dementia Research, Nathan Kline Institute, New York University School of Medicine, 140 Old Orangeburg Rd, Bldg 39, Orangeburg, NY 10962, USA
    Am J Pathol 173:665-81. 2008
    ..Our findings establish apoptosis as a mode of neuronal cell death in aging PS/APP mice and identify the cross talk between autophagy and apoptosis, which influences neuronal survival in AD-related neurodegeneration...
  18. pmc Protective mechanisms by cystatin C in neurodegenerative diseases
    Sebastien Gauthier
    Nathan S Kline Institute, Orangeburg, NY 10962, USA
    Front Biosci (Schol Ed) 3:541-54. 2011
    ..These data suggest that CysC is a therapeutic candidate that can potentially prevent brain damage and neurodegeneration...
  19. pmc Glutamatergic Transmission Aberration: A Major Cause of Behavioral Deficits in a Murine Model of Down's Syndrome
    Gurjinder Kaur
    Nathan S Kline Institute, Orangeburg, New York, 10962, Department of Child and Adolescent Psychiatry, Department of Psychiatry, Department of Biochemistry and Molecular Pharmacology, and Department of Physiology and Neuroscience, NYU Langone School of Medicine, New York, New York, 10016, and Department of Psychiatry, College of Physicians and Surgeons, Columbia University, New York, New York 10032
    J Neurosci 34:5099-106. 2014
    ..Thus, these findings suggest that glutamatergic deficits have a significant role in causing intellectual disabilities in DS. ..
  20. pmc Reversal of autophagy dysfunction in the TgCRND8 mouse model of Alzheimer's disease ameliorates amyloid pathologies and memory deficits
    Dun Sheng Yang
    Center for Dementia Research, Nathan Kline Institute, Orangeburg, NY 10962, USA
    Brain 134:258-77. 2011
    ..Our findings support the pathogenic significance of autophagic-lysosomal dysfunction in Alzheimer's disease and indicate the potential value of restoring normal autophagy as an innovative therapeutic strategy for Alzheimer's disease...
  21. pmc Early endosomal abnormalities and cholinergic neuron degeneration in amyloid-β protein precursor transgenic mice
    Jennifer H K Choi
    Nathan S Kline Institute, Orangeburg, NY 10962, USA
    J Alzheimers Dis 34:691-700. 2013
    ....
  22. pmc Cystatin C protects neuronal cells from amyloid-beta-induced toxicity
    Belen Tizon
    Nathan S Kline Institute, Orangeburg, NY, USA
    J Alzheimers Dis 19:885-94. 2010
    ..Therapeutic manipulation of CysC levels, resulting in slightly higher concentrations than physiological could protect neuronal cells from cell death in AD...
  23. pmc Olfactory dysfunction correlates with amyloid-beta burden in an Alzheimer's disease mouse model
    Daniel W Wesson
    Emotional Brain Institute and Center for Dementia Research, Nathan S Kline Institute for Psychiatric Research, Orangeburg, New York 10962, USA
    J Neurosci 30:505-14. 2010
    ..Furthermore, these results present the odor cross-habituation test as a powerful behavioral assay, which reflects Abeta deposition and thus may serve to monitor the efficacy of therapies aimed at reducing Abeta...
  24. pmc Systemic pathology in aged mouse models of Down's syndrome and Alzheimer's disease
    Seymour Levine
    Center for Dementia Research, Nathan S Kline Institute, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA
    Exp Mol Pathol 86:18-22. 2009
    ..The occurrence of lymphomas in mouse DS models is of interest in relation to the increased incidence of malignant conditions in human DS...
  25. pmc Sensory network dysfunction, behavioral impairments, and their reversibility in an Alzheimer's β-amyloidosis mouse model
    Daniel W Wesson
    Emotional Brain Institute, Nathan S Kline Institute for Psychiatric Research, Orangeburg, New York 10962, USA
    J Neurosci 31:15962-71. 2011
    ....
  26. ncbi request reprint Overexpression of human cystatin C in transgenic mice does not affect levels of endogenous brain amyloid Beta Peptide
    Monika Pawlik
    Department of Pharmacology, New York University School of Medicine, New York, NY, 10016, USA
    J Mol Neurosci 22:13-8. 2004
    ..Thus, in vivo overexpression of human cystatin C does not affect Abeta levels in mice that do not deposit Abeta...
  27. doi request reprint Murine cerebrovascular cells as a cell culture model for cerebral amyloid angiopathy: isolation of smooth muscle and endothelial cells from mouse brain
    Sebastien A Gauthier
    Department of Psychiatry, New York University School of Medicine, New York, NY, USA
    Methods Mol Biol 849:261-74. 2012
    ..Finally, we compare our methods with protocols designed to isolate and maintain human cerebrovascular cell cultures...
  28. pmc Mechanisms of neural and behavioral dysfunction in Alzheimer's disease
    Daniel W Wesson
    Emotional Brain Institute, Nathan S Kline Institute for Psychiatric Research, New York University School of Medicine, Orangeburg, NY 10962, USA
    Mol Neurobiol 43:163-79. 2011
    ....
  29. ncbi request reprint Purification of human wild-type or variant cystatin C from conditioned media of transfected cells
    Frances Prelli
    Department of Pathology, New York University School of Medicine, NY, USA
    Methods Mol Biol 299:221-6. 2005
    ..Following native purification conditions, variant cystatin C has a distinct structure compared to the wild-type protein...
  30. pmc Proteins that bind to the RERMS region of beta amyloid precursor protein
    Monika Pawlik
    Nathan Kline Institute, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA
    Biochem Biophys Res Commun 355:907-12. 2007
    ..Because both APP and hCRMP-2 promote neuronal outgrowth and use a common signaling pathway, APP could be acting through a semaphorin receptor as well...
  31. ncbi request reprint Murine cerebrovascular cells as a cell culture model for cerebral amyloid angiopathy: isolation of smooth muscle and endothelial cells from mouse brain
    Sonia S Jung
    Center for Dementia Research, Nathan S Kline Institute for Psychiatric Research, Orangeburg, NY, USA
    Methods Mol Biol 299:211-9. 2005
    ....
  32. ncbi request reprint Axonal transport of British and Danish amyloid peptides via secretory vesicles
    Seung Il Choi
    Department of Pathology, New York University School of Medicine, New York, New York, USA
    FASEB J 18:373-5. 2004
    ....
  33. ncbi request reprint Cystatin C modulates cerebral beta-amyloidosis
    Stephan A Kaeser
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Otfried Muller Strasse 27, D 72076 Tubingen, Germany
    Nat Genet 39:1437-9. 2007
    ..Our results suggest that cystatin C concentrations modulate cerebral amyloidosis risk and provide an opportunity for genetic risk assessment and therapeutic interventions...
  34. ncbi request reprint Alzheimer's presenilin 1 modulates sorting of APP and its carboxyl-terminal fragments in cerebral neurons in vivo
    Sam Gandy
    Farber Institute for Neurosciences and the Department of Neurology, Thomas Jefferson University, Philadelphia, Pennsylvania, USA
    J Neurochem 102:619-26. 2007
    ..The chimera experiment suggests that TGN-enrichment of a beta-/gamma-secretase substrate may play an integral role in the action of mutant PS1 to elevate brain levels of Abeta42...

Research Grants9

  1. Animal models for cerebral amyloid angiopathy
    Efrat Levy; Fiscal Year: 2006
    ..The proposed animal models are crucial for understanding the etiology of cerebral amyloid angiopathy and hemorrhage and for the development of rational therapeutic interventions. ..
  2. BETAAPP MODULATION BY THE ADAPTER PROTEINS FE65 AND X11
    Efrat Levy; Fiscal Year: 2000
    ..Manipulating the interaction of Beta-APP with an effector protein, such as X11 or Fe65, may provide a novel approach for the pharmacological modulation of Beta-APP processing in Alzheimer's disease. ..
  3. BETAAPP MODULATION BY THE ADAPTER PROTEINS FE65 AND X11
    Efrat Levy; Fiscal Year: 2001
    ..Manipulating the interaction of Beta-APP with an effector protein, such as X11 or Fe65, may provide a novel approach for the pharmacological modulation of Beta-APP processing in Alzheimer's disease. ..
  4. BETAAPP MODULATION BY THE ADAPTER PROTEINS FE65 AND X11
    Efrat Levy; Fiscal Year: 2002
    ..Manipulating the interaction of Beta-APP with an effector protein, such as X11 or Fe65, may provide a novel approach for the pharmacological modulation of Beta-APP processing in Alzheimer's disease. ..
  5. Animal models for cerebral amyloid angiopathy
    Efrat Levy; Fiscal Year: 2002
    ..The proposed animal models are crucial for understanding the etiology of cerebral amyloid angiopathy and hemorrhage and for the development of rational therapeutic interventions. ..
  6. Animal models for cerebral amyloid angiopathy
    Efrat Levy; Fiscal Year: 2003
    ..The proposed animal models are crucial for understanding the etiology of cerebral amyloid angiopathy and hemorrhage and for the development of rational therapeutic interventions. ..
  7. BETAAPP MODULATION BY THE ADAPTER PROTEINS FE65 AND X11
    Efrat Levy; Fiscal Year: 2003
    ..Manipulating the interaction of Beta-APP with an effector protein, such as X11 or Fe65, may provide a novel approach for the pharmacological modulation of Beta-APP processing in Alzheimer's disease. ..
  8. Animal models for cerebral amyloid angiopathy
    Efrat Levy; Fiscal Year: 2004
    ..The proposed animal models are crucial for understanding the etiology of cerebral amyloid angiopathy and hemorrhage and for the development of rational therapeutic interventions. ..
  9. Animal models for cerebral amyloid angiopathy
    Efrat Levy; Fiscal Year: 2005
    ..The proposed animal models are crucial for understanding the etiology of cerebral amyloid angiopathy and hemorrhage and for the development of rational therapeutic interventions. ..