Eileen M McGowan
Affiliation: Mayo Clinic
- Abeta42 is essential for parenchymal and vascular amyloid deposition in miceEileen 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...
- Anti-Abeta42- and anti-Abeta40-specific mAbs attenuate amyloid deposition in an Alzheimer disease mouse modelYona 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...
- A decade of modeling Alzheimer's disease in transgenic miceEileen 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...
- BRI2 inhibits amyloid beta-peptide precursor protein processing by interfering with the docking of secretases to the substrateShuji 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...
- Transgenic Mice Depositing Individual AB peptidesEileen 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. ..