Ablation of Cellular Prion Protein Does Not Ameliorate Abnormal Neural Network Activity or Cognitive Dysfunction in the J20 Line of Human Amyloid Precursor Protein Transgenic Mice
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L. Mucke | M. Cissé | Kaitlyn Ho | Pascal E. Sanchez | Daniel H. Kim | Gui-qiu Yu | M. Cissé | P. Sanchez
[1] L. Mucke,et al. Amyloid-β/Fyn–Induced Synaptic, Network, and Cognitive Impairments Depend on Tau Levels in Multiple Mouse Models of Alzheimer's Disease , 2011, The Journal of Neuroscience.
[2] Julie Harris,et al. Reversing EphB2 depletion rescues cognitive functions in Alzheimer model , 2011, Nature.
[3] R. Malinow,et al. The prion protein as a receptor for amyloid-β , 2010, Nature.
[4] J. Falsig,et al. Prion protein and Aβ-related synaptic toxicity impairment , 2010, EMBO Molecular Medicine.
[5] L. Mucke,et al. Amyloid-β–induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networks , 2010, Nature Neuroscience.
[6] W. Klein,et al. Deleterious Effects of Amyloid β Oligomers Acting as an Extracellular Scaffold for mGluR5 , 2010, Neuron.
[7] K. Zahs,et al. Probing the Biology of Alzheimer's Disease in Mice , 2010, Neuron.
[8] S. Strittmatter,et al. Memory Impairment in Transgenic Alzheimer Mice Requires Cellular Prion Protein , 2010, The Journal of Neuroscience.
[9] T. Zako,et al. Amyloid oligomers: formation and toxicity of Aβ oligomers , 2010, The FEBS journal.
[10] M. Gobbi,et al. Synthetic amyloid-β oligomers impair long-term memory independently of cellular prion protein , 2010, Proceedings of the National Academy of Sciences.
[11] Julie A. Harris,et al. Many Neuronal and Behavioral Impairments in Transgenic Mouse Models of Alzheimer's Disease Are Independent of Caspase Cleavage of the Amyloid Precursor Protein , 2010, The Journal of Neuroscience.
[12] O. Arancio,et al. MAPK, β-amyloid and synaptic dysfunction: the role of RAGE , 2009, Expert review of neurotherapeutics.
[13] G. Zamponi. Faculty Opinions recommendation of Cellular prion protein mediates impairment of synaptic plasticity by amyloid-beta oligomers. , 2009 .
[14] Sylvain Rheims,et al. Amyloid β-Induced Neuronal Hyperexcitability Triggers Progressive Epilepsy , 2009, The Journal of Neuroscience.
[15] John W. Gilbert,et al. Cellular Prion Protein Mediates Impairment of Synaptic Plasticity by Amyloid-β Oligomers , 2009, Nature.
[16] L. Mucke,et al. Neprilysin Overexpression Inhibits Plaque Formation But Fails to Reduce Pathogenic Aβ Oligomers and Associated Cognitive Deficits in Human Amyloid Precursor Protein Transgenic Mice , 2009, The Journal of Neuroscience.
[17] L. Mucke,et al. Phospholipase A2 reduction ameliorates cognitive deficits in a mouse model of Alzheimer's disease , 2008, Nature Neuroscience.
[18] A. Aguzzi,et al. The prion's elusive reason for being. , 2008, Annual review of neuroscience.
[19] L. Mucke,et al. Enkephalin Elevations Contribute to Neuronal and Behavioral Impairments in a Transgenic Mouse Model of Alzheimer's Disease , 2008, The Journal of Neuroscience.
[20] Anatol C. Kreitzer,et al. Aberrant Excitatory Neuronal Activity and Compensatory Remodeling of Inhibitory Hippocampal Circuits in Mouse Models of Alzheimer's Disease , 2007, Neuron.
[21] A. Aguzzi,et al. Enhanced susceptibility of Prnp‐deficient mice to kainate‐induced seizures, neuronal apoptosis, and death: Role of AMPA/kainate receptors , 2007, Journal of neuroscience research.
[22] L. Mucke,et al. Accelerating Amyloid-β Fibrillization Reduces Oligomer Levels and Functional Deficits in Alzheimer Disease Mouse Models* , 2007, Journal of Biological Chemistry.
[23] L. Mucke,et al. Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model , 2007, Science.
[24] L. Mucke,et al. Fyn Kinase Induces Synaptic and Cognitive Impairments in a Transgenic Mouse Model of Alzheimer's Disease , 2005, The Journal of Neuroscience.
[25] Kefei Chen,et al. Behavioral phenotypes of amyloid‐based genetically modified mouse models of Alzheimer's disease , 2005, Genes, brain, and behavior.
[26] L. Mucke,et al. Fyn Kinase Modulates Synaptotoxicity, But Not Aberrant Sprouting, in Human Amyloid Precursor Protein Transgenic Mice , 2004, The Journal of Neuroscience.
[27] A. Sakamoto,et al. Cellular Prion Protein: Implications in Seizures and Epilepsy , 2002, Cellular and Molecular Neurobiology.
[28] J. David Sweatt,et al. β-Amyloid Peptide Activates α7 Nicotinic Acetylcholine Receptors Expressed in Xenopus Oocytes* , 2002, The Journal of Biological Chemistry.
[29] Kang Hu,et al. High-Level Neuronal Expression of Aβ1–42 in Wild-Type Human Amyloid Protein Precursor Transgenic Mice: Synaptotoxicity without Plaque Formation , 2000, The Journal of Neuroscience.
[30] O. Amaral,et al. Increased Sensitivity to Seizures in Mice Lacking Cellular Prion Protein , 1999, Epilepsia.
[31] R. Motter,et al. Amyloid precursor protein processing and Aβ42 deposition in a transgenic mouse model of Alzheimer disease , 1997 .
[32] L. Mucke,et al. Levels and Alternative Splicing of Amyloid β Protein Precursor (APP) Transcripts in Brains of APP Transgenic Mice and Humans with Alzheimer's Disease (*) , 1995, The Journal of Biological Chemistry.
[33] S. Prusiner,et al. Normal development and behaviour of mice lacking the neuronal cell-surface PrP protein , 1992, Nature.