Manuel Buttini

Summary

Affiliation: Elan Pharmaceuticals
Country: USA

Publications

  1. pmc Cellular source of apolipoprotein E4 determines neuronal susceptibility to excitotoxic injury in transgenic mice
    Manuel Buttini
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158 2261, USA
    Am J Pathol 177:563-9. 2010
  2. ncbi Beta-amyloid immunotherapy prevents synaptic degeneration in a mouse model of Alzheimer's disease
    Manuel Buttini
    Elan Pharmaceuticals, South San Francisco, California 94080, USA
    J Neurosci 25:9096-101. 2005
  3. ncbi Partial reduction of BACE1 has dramatic effects on Alzheimer plaque and synaptic pathology in APP Transgenic Mice
    Lisa McConlogue
    Department of Biology, Elan Pharmaceuticals, South San Francisco, California 94080, USA
    J Biol Chem 282:26326-34. 2007
  4. ncbi Modulation of Alzheimer-like synaptic and cholinergic deficits in transgenic mice by human apolipoprotein E depends on isoform, aging, and overexpression of amyloid beta peptides but not on plaque formation
    Manuel Buttini
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94141 9100, USA
    J Neurosci 22:10539-48. 2002
  5. ncbi Neuron-specific apolipoprotein e4 proteolysis is associated with increased tau phosphorylation in brains of transgenic mice
    Walter J Brecht
    Gladstone Institute of Neurological Disease, San Francisco, California 94141 9100, USA
    J Neurosci 24:2527-34. 2004
  6. doi Neutralization of soluble, synaptotoxic amyloid β species by antibodies is epitope specific
    Wagner Zago
    Janssen Alzheimer Immunotherapy Research and Development, South San Francisco, CA 94080, USA
    J Neurosci 32:2696-702. 2012
  7. ncbi Mice as models: transgenic approaches and Alzheimer's disease
    Dora Games
    Elan Pharmaceuticals, 800 Gateway Blvd, South San Francisco, CA 94080, USA
    J Alzheimers Dis 9:133-49. 2006
  8. pmc Morphological characterization of Thioflavin-S-positive amyloid plaques in transgenic Alzheimer mice and effect of passive Abeta immunotherapy on their clearance
    Thierry Bussiere
    Elan Pharmaceuticals, South San Francisco, California, USA
    Am J Pathol 165:987-95. 2004
  9. ncbi BACE1 gene deletion: impact on behavioral function in a model of Alzheimer's disease
    Dione Kobayashi
    Rinat Neurosciences, 230 East Grand Avenue, South San Francisco, CA 94080, USA
    Neurobiol Aging 29:861-73. 2008
  10. ncbi Androgens protect against apolipoprotein E4-induced cognitive deficits
    Jacob Raber
    Gladstone Institute of Neurological Disease and Department of Neurology, University of California, San Francisco, California 94141, USA
    J Neurosci 22:5204-9. 2002

Detail Information

Publications13

  1. pmc Cellular source of apolipoprotein E4 determines neuronal susceptibility to excitotoxic injury in transgenic mice
    Manuel Buttini
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158 2261, USA
    Am J Pathol 177:563-9. 2010
    ..Thus, an imbalance between astrocytic (excitoprotective) and neuronal (neurotoxic) apoE4 expression may increase susceptibility to diverse neurological diseases involving excitotoxic mechanisms...
  2. ncbi Beta-amyloid immunotherapy prevents synaptic degeneration in a mouse model of Alzheimer's disease
    Manuel Buttini
    Elan Pharmaceuticals, South San Francisco, California 94080, USA
    J Neurosci 25:9096-101. 2005
    ....
  3. ncbi Partial reduction of BACE1 has dramatic effects on Alzheimer plaque and synaptic pathology in APP Transgenic Mice
    Lisa McConlogue
    Department of Biology, Elan Pharmaceuticals, South San Francisco, California 94080, USA
    J Biol Chem 282:26326-34. 2007
    ....
  4. ncbi Modulation of Alzheimer-like synaptic and cholinergic deficits in transgenic mice by human apolipoprotein E depends on isoform, aging, and overexpression of amyloid beta peptides but not on plaque formation
    Manuel Buttini
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94141 9100, USA
    J Neurosci 22:10539-48. 2002
    ..Thus, apoE3, but not apoE4, delays age- and Abeta-dependent synaptic deficits through a plaque-independent mechanism. This difference could contribute to the differential effects of apoE isoforms on the risk and onset of AD...
  5. ncbi Neuron-specific apolipoprotein e4 proteolysis is associated with increased tau phosphorylation in brains of transgenic mice
    Walter J Brecht
    Gladstone Institute of Neurological Disease, San Francisco, California 94141 9100, USA
    J Neurosci 24:2527-34. 2004
    ..Neuron-specific proteolytic cleavage of apoE4 is associated with increased phosphorylation of tau and may play a key role in the development of AD-related neuronal deficits...
  6. doi Neutralization of soluble, synaptotoxic amyloid β species by antibodies is epitope specific
    Wagner Zago
    Janssen Alzheimer Immunotherapy Research and Development, South San Francisco, CA 94080, USA
    J Neurosci 32:2696-702. 2012
    ..These results, taken with prior studies, suggest that N-terminal anti-Aβ antibodies effectively interact with both soluble and insoluble forms of Aβ and therefore appear particularly well suited for testing the Aβ hypothesis of AD...
  7. ncbi Mice as models: transgenic approaches and Alzheimer's disease
    Dora Games
    Elan Pharmaceuticals, 800 Gateway Blvd, South San Francisco, CA 94080, USA
    J Alzheimers Dis 9:133-49. 2006
    ..As a result, we may see containment or even the elimination of AD in the near future as a direct consequence of these advances...
  8. pmc Morphological characterization of Thioflavin-S-positive amyloid plaques in transgenic Alzheimer mice and effect of passive Abeta immunotherapy on their clearance
    Thierry Bussiere
    Elan Pharmaceuticals, South San Francisco, California, USA
    Am J Pathol 165:987-95. 2004
    ..Our results show that distinct morphological types of plaques are differentially cleared depending upon the isotype of the antibody...
  9. ncbi BACE1 gene deletion: impact on behavioral function in a model of Alzheimer's disease
    Dione Kobayashi
    Rinat Neurosciences, 230 East Grand Avenue, South San Francisco, CA 94080, USA
    Neurobiol Aging 29:861-73. 2008
    ..These results suggest that while excess Abeta is functionally pathological, BACE1-mediated processing of APP and other substrates play a role in "normal" learning, memory and sensorimotor processes...
  10. ncbi Androgens protect against apolipoprotein E4-induced cognitive deficits
    Jacob Raber
    Gladstone Institute of Neurological Disease and Department of Neurology, University of California, San Francisco, California 94141, USA
    J Neurosci 22:5204-9. 2002
    ..Our findings suggest that apoE4 contributes to cognitive decline by reducing AR levels in the brain, and that stimulating AR-dependent pathways can reverse apoE4-induced cognitive deficits...
  11. pmc Increased T cell recruitment to the CNS after amyloid beta 1-42 immunization in Alzheimer's mice overproducing transforming growth factor-beta 1
    Marion S Buckwalter
    Neurology and Neurological Sciences, Stanford University, Stanford, California 94305, USA
    J Neurosci 26:11437-41. 2006
    ..Likewise, levels of TGF-beta1 or other immune factors in brains of AD patients may influence the response to Abeta(1-42) immunization...
  12. pmc RAGE potentiates Abeta-induced perturbation of neuronal function in transgenic mice
    Ottavio Arancio
    Department of Psychiatry, Physiology and Neuroscience, Dementia Research Center, Nathan Kline Institute, New York University School of Medicine, NY 10032, USA
    EMBO J 23:4096-105. 2004
    ..These data indicate that RAGE is a cofactor for Abeta-induced neuronal perturbation in a model of Alzheimer's-type pathology, and suggest its potential as a therapeutic target to ameliorate cellular dysfunction...
  13. pmc Evaluation of alpha-synuclein immunohistochemical methods used by invited experts
    Thomas G Beach
    Civin Laboratory for Neuropathology, Sun Health Research Institute, 10515 West Santa Fe Drive, Sun City, AZ 85351, USA
    Acta Neuropathol 116:277-88. 2008
    ..Some methods, however, achieved relatively high sensitivities with optimized formic acid protocols combined with a hydrolytic step. One method was developed that allows high sensitivity with commercially available reagents...