Eileen M McGowan

Summary

Affiliation: Mayo Clinic
Country: USA

Publications

  1. ncbi Abeta42 is essential for parenchymal and vascular amyloid deposition in mice
    Eileen McGowan
    Department Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 32224, USA
    Neuron 47:191-9. 2005
  2. ncbi Anti-Abeta42- and anti-Abeta40-specific mAbs attenuate amyloid deposition in an Alzheimer disease mouse model
    Yona Levites
    Department of Neuroscience, Mayo Clinic, Mayo Clinic College of Medicine, Jacksonville, Florida 32224, USA
    J Clin Invest 116:193-201. 2006
  3. ncbi A decade of modeling Alzheimer's disease in transgenic mice
    Eileen McGowan
    Department of Neuroscience, Mayo Clinic College of Medicine, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    Trends Genet 22:281-9. 2006
  4. ncbi BRI2 inhibits amyloid beta-peptide precursor protein processing by interfering with the docking of secretases to the substrate
    Shuji Matsuda
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Neurosci 28:8668-76. 2008

Research Grants

  1. Transgenic Mice Depositing Individual AB peptides
    Eileen McGowan; Fiscal Year: 2006

Collaborators

Detail Information

Publications4

  1. ncbi Abeta42 is essential for parenchymal and vascular amyloid deposition in mice
    Eileen McGowan
    Department Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 32224, USA
    Neuron 47:191-9. 2005
    ..These data establish that Abeta1-42 is essential for amyloid deposition in the parenchyma and also in vessels...
  2. ncbi Anti-Abeta42- and anti-Abeta40-specific mAbs attenuate amyloid deposition in an Alzheimer disease mouse model
    Yona Levites
    Department of Neuroscience, Mayo Clinic, Mayo Clinic College of Medicine, Jacksonville, Florida 32224, USA
    J Clin Invest 116:193-201. 2006
    ..These data suggest that selective targeting of Abeta42 or Abeta40 may be an effective strategy to prevent amyloid deposition, but may have limited benefit in a therapeutic setting...
  3. ncbi A decade of modeling Alzheimer's disease in transgenic mice
    Eileen McGowan
    Department of Neuroscience, Mayo Clinic College of Medicine, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    Trends Genet 22:281-9. 2006
    ..The relationship between these lesions, neurodegeneration and development of the clinical syndrome will be explored...
  4. ncbi BRI2 inhibits amyloid beta-peptide precursor protein processing by interfering with the docking of secretases to the substrate
    Shuji Matsuda
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Neurosci 28:8668-76. 2008
    ..Alterations of BRI2 by gene targeting or transgenic expression regulate Abeta levels and AD pathology in mouse models of AD. Competitive inhibition of APP processing by BRI2 may provide a new approach to AD therapy and prevention...

Research Grants4

  1. Transgenic Mice Depositing Individual AB peptides
    Eileen McGowan; Fiscal Year: 2006
    ..3). To assess whether behavioral alterations occur in BRI-Abeta40 and BRI-Abeta42 mice and determine the relationship of any observed behavioral alterations with the pathological changes observed. ..