William J Netzer

Summary

Affiliation: The Rockefeller University
Country: USA

Publications

  1. pmc Lowering beta-amyloid levels rescues learning and memory in a Down syndrome mouse model
    William J Netzer
    Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, New York, USA
    PLoS ONE 5:e10943. 2010
  2. pmc Presenilin-1 uses phospholipase D1 as a negative regulator of beta-amyloid formation
    Dongming Cai
    Laboratory of Molecular and Cellular Neuroscience, and Fisher Center for Research on Alzheimer Disease, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 103:1941-6. 2006
  3. pmc Gamma-secretase activating protein is a therapeutic target for Alzheimer's disease
    Gen He
    Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, 1230 York Avenue, New York, New York 10065, USA
    Nature 467:95-8. 2010
  4. pmc Phospholipase D1 corrects impaired betaAPP trafficking and neurite outgrowth in familial Alzheimer's disease-linked presenilin-1 mutant neurons
    Dongming Cai
    Laboratory of Molecular and Cellular Neuroscience, and Fisher Center for Research on Alzheimer Disease, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 103:1936-40. 2006
  5. pmc Dynamin 1 regulates amyloid generation through modulation of BACE-1
    Li Zhu
    Department of Neurology and Alzheimer s Disease Research Center, Mount Sinai School of Medicine, New York, New York, United States of America
    PLoS ONE 7:e45033. 2012
  6. pmc Gleevec inhibits beta-amyloid production but not Notch cleavage
    William J Netzer
    Fisher Center for Research on Alzheimer s Disease, Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 100:12444-9. 2003
  7. pmc Chaperones increase association of tau protein with microtubules
    Fei Dou
    Fisher Center for Research on Alzheimer s Disease, Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 100:721-6. 2003

Collaborators

Detail Information

Publications7

  1. pmc Lowering beta-amyloid levels rescues learning and memory in a Down syndrome mouse model
    William 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...
  2. pmc Presenilin-1 uses phospholipase D1 as a negative regulator of beta-amyloid formation
    Dongming Cai
    Laboratory of Molecular and Cellular Neuroscience, and Fisher Center for Research on Alzheimer Disease, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 103:1941-6. 2006
    ..The data indicate that overexpression of PLD1 decreases, and down-regulation of PLD1 increases, the catalytic activity, and the association of the subunits, of gamma-secretase...
  3. pmc Gamma-secretase activating protein is a therapeutic target for Alzheimer's disease
    Gen He
    Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, 1230 York Avenue, New York, New York 10065, USA
    Nature 467:95-8. 2010
    ..Thus, GSAP can serve as an amyloid-beta-lowering therapeutic target without affecting other key functions of gamma-secretase...
  4. pmc Phospholipase D1 corrects impaired betaAPP trafficking and neurite outgrowth in familial Alzheimer's disease-linked presenilin-1 mutant neurons
    Dongming Cai
    Laboratory of Molecular and Cellular Neuroscience, and Fisher Center for Research on Alzheimer Disease, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 103:1936-40. 2006
    ..The impaired neurite outgrowth capacity in FAD mutant neurons was corrected by introducing PLD1 into these cells. The results indicate that PLD1 may represent a therapeutic target for rescuing compromised neuronal function in AD...
  5. pmc Dynamin 1 regulates amyloid generation through modulation of BACE-1
    Li Zhu
    Department of Neurology and Alzheimer s Disease Research Center, Mount Sinai School of Medicine, New York, New York, United States of America
    PLoS ONE 7:e45033. 2012
    ..Dynamin, an important adaptor protein that controls sorting of many molecules, has recently been associated with AD but its functions remain controversial. Here we studied possible roles for dynamin 1 (dyn1) in Aβ biogenesis...
  6. pmc Gleevec inhibits beta-amyloid production but not Notch cleavage
    William J Netzer
    Fisher Center for Research on Alzheimer s Disease, Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 100:12444-9. 2003
    ..The efficacy of STI571 in reducing Abeta without affecting Notch-1 cleavage may prove useful as a basis for developing novel therapies for Alzheimer's disease...
  7. pmc Chaperones increase association of tau protein with microtubules
    Fei Dou
    Fisher Center for Research on Alzheimer s Disease, Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 100:721-6. 2003
    ..Our results suggest that up-regulation of molecular chaperones may suppress formation of neurofibrillary tangles by partitioning tau into a productive folding pathway and thereby preventing tau aggregation...