Massive CA1/2 Neuronal Loss with Intraneuronal and N-Terminal Truncated Aβ42 Accumulation in a Novel Alzheimer Transgenic Model

This publication has 48 references indexed in Scilit:

• Intraneuronal APP/Aβ Trafficking and Plaque Formation in β‐Amyloid Precursor Protein and Presenilin‐1 Transgenic Mice
  Brain Pathology, 2002
• BACE1 interacts with nicastrin
  Biochemical and Biophysical Research Communications, 2002
• Normal brain development in PS1 hypomorphic mice with markedly reduced γ-secretase cleavage of βAPP
  Neurobiology of Aging, 2002
• Glu11 Site Cleavage and N-Terminally Truncated Aβ Production upon BACE Overexpression
  Biochemistry, 2002
• Brain Aβ amyloidosis in APPsw mice induces accumulation of presenilin-1 and tau
  The Journal of Pathology, 2001
• Amyloid β Protein Starting Pyroglutamate at Position 3 Is a Major Component of the Amyloid Deposits in the Alzheimer's Disease Brain
  Biochemical and Biophysical Research Communications, 2000
• Neuronal cell death in Alzheimer's disease correlates with apoE uptake and intracellular Abeta stabilization.
  Journal of Clinical Investigation, 1997
• Two novel (M233T and ρ278T) presenilin-1 mutations in early-onset Alzheimerʼs disease pedigrees and preliminary evidence for association of presenilin-1 mutations with a novel phenotype
  NeuroReport, 1997
• Amino- and carboxyl-terminal heterogeneity of β-amyloid peptides deposited in human brain
  Neuroscience Letters, 1996
• A novel presenilin 1 mutation resulting in familial Alzheimerʼs disease with an onset age of 29 years
  NeuroReport, 1996