Neurofibrillary tangle formation by introducing wild-type human tau into APP transgenic mice

[1]  Pasko Rakic,et al.  A Transgenic Alzheimer Rat with Plaques, Tau Pathology, Behavioral Impairment, Oligomeric Aβ, and Frank Neuronal Loss , 2013, The Journal of Neuroscience.

[2]  Katsuhiro Yoshikawa,et al.  Modeling Alzheimer's disease with iPSCs reveals stress phenotypes associated with intracellular Aβ and differential drug responsiveness. , 2013, Cell stem cell.

[3]  W. Klein.  Synaptotoxic amyloid-β oligomers: a molecular basis for the cause, diagnosis, and treatment of Alzheimer's disease? , 2012, Journal of Alzheimer's disease : JAD.

[4]  H. Nakayama,et al.  Neurofibrillary Tangles and the Deposition of a Beta Amyloid Peptide with a Novel N-Terminal Epitope in the Brains of Wild Tsushima Leopard Cats , 2012, PloS one.

[5]  Y. Une,et al.  Beta Amyloid Deposition and Neurofibrillary Tangles Spontaneously Occur in the Brains of Captive Cheetahs (Acinonyx jubatus) , 2012, Veterinary pathology.

[6]  R. Nussinov,et al.  Synergistic Interactions between Repeats in Tau Protein and Aβ Amyloids May Be Responsible for Accelerated Aggregation via Polymorphic States , 2011, Biochemistry.

[7]  J. Trojanowski,et al.  The acetylation of tau inhibits its function and promotes pathological tau aggregation. , 2011, Nature communications.

[8]  D. Selkoe,et al.  Soluble amyloid β-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration , 2011, Proceedings of the National Academy of Sciences.

[9]  K. Ando,et al.  Accelerated human mutant tau aggregation by knocking out murine tau in a transgenic mouse model. , 2011, The American journal of pathology.

[10]  D. Westaway,et al.  Amyloid β accelerates phosphorylation of tau and neurofibrillary tangle formation in an amyloid precursor protein and tau double‐transgenic mouse model , 2010, Journal of neuroscience research.

[11]  V. Haroutunian,et al.  Acetylation of Tau Inhibits Its Degradation and Contributes to Tauopathy , 2010, Neuron.

[12]  John Q Trojanowski,et al.  A{beta} accelerates the spatiotemporal progression of tau pathology and augments tau amyloidosis in an Alzheimer mouse model. , 2010, The American journal of pathology.

[13]  Jürgen Götz,et al.  Dendritic Function of Tau Mediates Amyloid-β Toxicity in Alzheimer's Disease Mouse Models , 2010, Cell.

[14]  J. Trojanowski,et al.  Synergistic Interactions between Aβ, Tau, and α-Synuclein: Acceleration of Neuropathology and Cognitive Decline , 2010, The Journal of Neuroscience.

[15]  Rie Teraoka,et al.  A Mouse Model of Amyloid β Oligomers: Their Contribution to Synaptic Alteration, Abnormal Tau Phosphorylation, Glial Activation, and Neuronal Loss In Vivo , 2010, The Journal of Neuroscience.

[16]  Rodrigo Morales,et al.  Molecular Cross Talk between Misfolded Proteins in Animal Models of Alzheimer's and Prion Diseases , 2010, The Journal of Neuroscience.

[17]  K. Yanagisawa,et al.  Alzheimer-type tau pathology in advanced aged nonhuman primate brains harboring substantial amyloid deposition , 2010, Brain Research.

[18]  R. Brandt,et al.  Divergent Pathways Mediate Spine Alterations and Cell Death Induced by Amyloid-β, Wild-Type Tau, and R406W Tau , 2009, The Journal of Neuroscience.

[19]  H. Steinhoff,et al.  Microtubule Binding and Trapping at the Tip of Neurites Regulate Tau Motion in Living Neurons , 2009, Traffic.

[20]  D. Dickson,et al.  Overexpression of wild-type murine tau results in progressive tauopathy and neurodegeneration. , 2009, The American journal of pathology.

[21]  Shaomin Li,et al.  Soluble Oligomers of Amyloid β Protein Facilitate Hippocampal Long-Term Depression by Disrupting Neuronal Glutamate Uptake , 2009, Neuron.

[22]  K. Ashe,et al.  Amyloid plaque and neurofibrillary tangle pathology in a regulatable mouse model of Alzheimer's disease. , 2008, The American journal of pathology.

[23]  E. Bigio,et al.  Alzheimer's disease-type neuronal tau hyperphosphorylation induced by Aβ oligomers , 2008, Neurobiology of Aging.

[24]  Giovanni Coppola,et al.  Tauopathy with paired helical filaments in an aged chimpanzee , 2008, The Journal of comparative neurology.

[25]  Yasuyoshi Watanabe,et al.  A new amyloid β variant favoring oligomerization in Alzheimer's‐type dementia , 2008, Annals of neurology.

[26]  H. Bujard,et al.  The Potential for β-Structure in the Repeat Domain of Tau Protein Determines Aggregation, Synaptic Decay, Neuronal Loss, and Coassembly with Endogenous Tau in Inducible Mouse Models of Tauopathy , 2008, The Journal of Neuroscience.

[27]  M. Staufenbiel,et al.  Induction of Tau Pathology by Intracerebral Infusion of Amyloid-β-Containing Brain Extract and by Amyloid-β Deposition in APP × Tau Transgenic Mice , 2007 .

[28]  C. Duyckaerts,et al.  Alzheimer disease models and human neuropathology: similarities and differences , 2007, Acta Neuropathologica.

[29]  S. Frank,et al.  Tauopathy models and human neuropathology: similarities and differences , 2007, Acta Neuropathologica.

[30]  Bernardo L Sabatini,et al.  Natural Oligomers of the Alzheimer Amyloid-β Protein Induce Reversible Synapse Loss by Modulating an NMDA-Type Glutamate Receptor-Dependent Signaling Pathway , 2007, The Journal of Neuroscience.

[31]  W. Klein,et al.  Aβ Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease , 2007, The Journal of Neuroscience.

[32]  Tetsuaki Arai,et al.  Abeta and tau form soluble complexes that may promote self aggregation of both into the insoluble forms observed in Alzheimer's disease. , 2006, Proceedings of the National Academy of Sciences of the United States of America.

[33]  I. Ferrer,et al.  Accelerated amyloid deposition, neurofibrillary degeneration and neuronal loss in double mutant APP/tau transgenic mice , 2005, Neurobiology of Disease.

[34]  A. Grover,et al.  Hyperphosphorylation-induced self assembly of murine tau: a comparison with human tau , 2005, Journal of Neural Transmission.

[35]  P. Davies,et al.  Hyperphosphorylation and aggregation of tau in mice expressing normal human tau isoforms , 2003, Journal of neurochemistry.

[36]  M. Mattson,et al.  Triple-Transgenic Model of Alzheimer's Disease with Plaques and Tangles Intracellular Aβ and Synaptic Dysfunction , 2003, Neuron.

[37]  H. Mori,et al.  Isoforms changes of tau protein during development in various species. , 2003, Brain research. Developmental brain research.

[38]  J. Hardy,et al.  Enhanced Neurofibrillary Degeneration in Transgenic Mice Expressing Mutant Tau and APP , 2001, Science.

[39]  J. Trojanowski,et al.  Age-dependent induction of congophilic neurofibrillary tau inclusions in tau transgenic mice. , 2001, The American journal of pathology.

[40]  R. Brandt,et al.  Interaction of Tau with the Neural Membrane Cortex Is Regulated by Phosphorylation at Sites That Are Modified in Paired Helical Filaments* , 2000, The Journal of Biological Chemistry.

[41]  H. Braak,et al.  Filamentous Tau Pathology in Nerve Cells, Astrocytes, and Oligodendrocytes of Aged Baboons , 2000, Journal of neuropathology and experimental neurology.

[42]  D. Mann,et al.  Deposition of beta-amyloid subtypes 40 and 42 differentiates dementia with Lewy bodies from Alzheimer disease. , 1999, Archives of neurology.

[43]  H. Geerts,et al.  Assembly of paired helical filaments from mouse tau: implications for the neurofibrillary pathology in transgenic mouse models for Alzheimer's disease , 1999, FEBS letters.

[44]  R. Brandt,et al.  Interaction of tau with the neural plasma membrane mediated by tau's amino-terminal projection domain , 1995, The Journal of cell biology.

[45]  K. Beyreuther,et al.  Amyloidogenicity of rodent and human βA4 sequences , 1993 .

[46]  N. Cairns,et al.  Tau proteins of alzheimer paired helical filaments: Abnormal phosphorylation of all six brain isoforms , 1992, Neuron.

[47]  P. Reddy,et al.  Abnormal interaction of oligomeric amyloid-β with phosphorylated tau: implications to synaptic dysfunction and neuronal damage. , 2013, Journal of Alzheimer's disease : JAD.

[48]  J. Hardy,et al.  Amyloid deposition as the central event in the aetiology of Alzheimer's disease. , 1991, Trends in pharmacological sciences.

[49]  A. Takashima,et al.  Neurodegenerative Disorder FTDP-17 e Related Tau Intron 10 D 16C / T Mutation Increases Tau Exon 10 Splicing and Causes Tauopathy in Transgenic Mice , 2022 .