ERK1/2 Activation Mediates Aβ Oligomer-induced Neurotoxicity via Caspase-3 Activation and Tau Cleavage in Rat Organotypic Hippocampal Slice Cultures

This publication has 62 references indexed in Scilit:

• The Generation of a 17 kDa Neurotoxic Fragment: An Alternative Mechanism by which Tau Mediates β-Amyloid-Induced Neurodegeneration
  Journal of Neuroscience, 2005
• Preserved synaptic vesicle recycling in hippocampal neurons in a mouse Alzheimer’s disease model
  Biochemical and Biophysical Research Communications, 2005
• Natural oligomers of the amyloid-β protein specifically disrupt cognitive function
  Nature Neuroscience, 2004
• Macrophage colony stimulatory factor and interferon‐γ trigger distinct mechanisms for augmentation of β‐amyloid‐induced microglia‐mediated neurotoxicity
  Journal of Neurochemistry, 2004
• Pathways towards and away from Alzheimer's disease
  Nature, 2004
• Unique Physicochemical Profile of β-Amyloid Peptide Variant Aβ1–40E22G Protofibrils: Conceivable Neuropathogen in Arctic Mutant Carriers
  Journal of Molecular Biology, 2004
• Apoptosis shifts to necrosis via intermediate types of cell death by a mechanism depending on c- myc and bcl-2 expression
  Cell and tissue research, 2004
• Soluble oligomeric Aβ disrupts the protein kinase C signaling pathway
  NeuroReport, 2004
• Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of Pathogenesis
  Science, 2003
• The 'Arctic' APP mutation (E693G) causes Alzheimer's disease by enhanced Aβ protofibril formation
  Nature Neuroscience, 2001