Long-term prevention of Alzheimer's disease-like behavioral deficits in PDAPP mice carrying a mutation in Asp664
暂无分享,去创建一个
D. Bredesen | V. Galvan | Surita Banwait | Wei Huang | Huidong Tang | Junli Zhang | O. Gorostiza | M. Ataie
[1] D. Bredesen,et al. Interaction of ASK1 and the β-amyloid precursor protein in a stress-signaling complex , 2007, Neurobiology of Disease.
[2] L. Mucke,et al. Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model , 2007, Science.
[3] Jacqueline N. Crawley,et al. What's Wrong With My Mouse? , 2007 .
[4] H. Baker,et al. Changes in transcription within the CA1 field of the hippocampus are associated with age-related spatial learning impairments , 2007, Neurobiology of Learning and Memory.
[5] S. Heinemann,et al. Deficits in Synaptic Transmission and Learning in Amyloid Precursor Protein (APP) Transgenic Mice Require C-Terminal Cleavage of APP , 2006, The Journal of Neuroscience.
[6] M. Sofroniew,et al. Essential protective roles of reactive astrocytes in traumatic brain injury. , 2006, Brain : a journal of neurology.
[7] D. Bredesen,et al. Aβ induces cell death by direct interaction with its cognate extracellular domain on APP (APP 597–624) , 2006, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[8] D. Bredesen,et al. Correction for Galvan et al., Reversal of Alzheimer's-like pathology and behavior in human APP transgenic mice by mutation of Asp664 , 2006, Proceedings of the National Academy of Sciences.
[9] Sun-Young Oh,et al. Visualization of APP dimerization and APP‐Notch2 heterodimerization in living cells using bimolecular fluorescence complementation , 2006, Journal of neurochemistry.
[10] A. Prochiantz,et al. SET protein (TAF1β, I2PP2A) is involved in neuronal apoptosis induced by an amyloid precursor protein cytoplasmic subdomain , 2005, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[11] D. Borchelt,et al. Environmental Enrichment Mitigates Cognitive Deficits in a Mouse Model of Alzheimer's Disease , 2005, The Journal of Neuroscience.
[12] Yaakov Stern,et al. Cognitive reserve: Implications for diagnosis and prevention of Alzheimer’s disease , 2004, Current Neurology and Neuroscience Reports.
[13] W. Streit,et al. Microglia and Alzheimer's disease pathogenesis , 2004, Journal of neuroscience research.
[14] C. Janus. Search strategies used by APP transgenic mice during navigation in the Morris water maze. , 2004, Learning & memory.
[15] E. Nestler,et al. Neurobehavioral assessment in the information age , 2004, Nature Neuroscience.
[16] R. Poland,et al. Reduced Immobility in the Forced Swim Test in Mice with a Targeted Deletion of the Leukemia Inhibitory Factor (LIF) Gene , 2004, Neuropsychopharmacology.
[17] C. Sandi,et al. Water maze learning and forebrain mRNA expression of the neural cell adhesion molecule L1 , 2004, Journal of neuroscience research.
[18] E. Masliah,et al. Amyloid β protein toxicity mediated by the formation of amyloid‐β protein precursor complexes , 2003 .
[19] R. Tanzi,et al. Caspase Activation Increases β-Amyloid Generation Independently of Caspase Cleavage of the β-Amyloid Precursor Protein (APP)* , 2003, Journal of Biological Chemistry.
[20] M. O’Connor-McCourt,et al. Substrate cleavage by caspases generates protein fragments with Smac/Diablo-like activities , 2003, Cell Death and Differentiation.
[21] D. Bredesen,et al. Caspase cleavage of the amyloid precursor protein modulates amyloid β‐protein toxicity , 2003, Journal of neurochemistry.
[22] Jacob Raber,et al. Neuronal depletion of calcium-dependent proteins in the dentate gyrus is tightly linked to Alzheimer's disease-related cognitive deficits , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[23] K. Miyazawa,et al. A Scaffold Protein JIP-1b Enhances Amyloid Precursor Protein Phosphorylation by JNK and Its Association with Kinesin Light Chain 1* , 2003, Journal of Biological Chemistry.
[24] A. Savonenko,et al. Protective Effect of Practice on Cognition during Aging: Implications for Predictive Characteristics of Performance and Efficacy of Practice , 2002, Neurobiology of Learning and Memory.
[25] R. Turner,et al. Synergistic Effects of Munc18a and X11 Proteins on Amyloid Precursor Protein Metabolism* , 2002, The Journal of Biological Chemistry.
[26] D. Bredesen,et al. Caspase cleavage of members of the amyloid precursor family of proteins , 2002, Journal of neurochemistry.
[27] D. Selkoe,et al. The Intracellular Domain of the β-Amyloid Precursor Protein Is Stabilized by Fe65 and Translocates to the Nucleus in a Notch-like Manner* , 2001, The Journal of Biological Chemistry.
[28] T. Hiraki,et al. c-Jun N-Terminal Kinase (JNK)-Interacting Protein-1b/Islet-Brain-1 Scaffolds Alzheimer's Amyloid Precursor Protein with JNK , 2001, The Journal of Neuroscience.
[29] S. Chandra,et al. The Amyloidogenic Pathway of Amyloid Precursor Protein (APP) Is Independent of Its Cleavage by Caspases* , 2001, The Journal of Biological Chemistry.
[30] Guiquan Chen,et al. A learning deficit related to age and β-amyloid plaques in a mouse model of Alzheimer's disease , 2000, Nature.
[31] Hsiao-Wen Chen,et al. Unusual spectral energy distribution of a galaxy previously reported to be at redshift 6.68 , 2000, Nature.
[32] L. Goldstein,et al. Axonal Transport of Amyloid Precursor Protein Is Mediated by Direct Binding to the Kinesin Light Chain Subunit of Kinesin-I , 2000, Neuron.
[33] 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.
[34] S. Chandra,et al. A second cytotoxic proteolytic peptide derived from amyloid β-protein precursor , 2000, Nature Medicine.
[35] Ramin Homayouni,et al. Disabled-1 Binds to the Cytoplasmic Domain of Amyloid Precursor-Like Protein 1 , 1999, The Journal of Neuroscience.
[36] Jonathan A. Cooper,et al. Phospholipids of Transmembrane Glycoproteins and to Domain Binds to the Internalization Signals The Disabled 1 Phosphotyrosine-Binding , 1999 .
[37] David Smith,et al. Involvement of Caspases in Proteolytic Cleavage of Alzheimer’s Amyloid-β Precursor Protein and Amyloidogenic Aβ Peptide Formation , 1999, Cell.
[38] R. Nicoll,et al. Plaque-independent disruption of neural circuits in Alzheimer's disease mouse models. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[39] David P. Wolfer,et al. Spatial Memory and Learning in Transgenic Mice: Fact or Artifact? , 1998, News in physiological sciences : an international journal of physiology produced jointly by the International Union of Physiological Sciences and the American Physiological Society.
[40] R. Morris. Developments of a water-maze procedure for studying spatial learning in the rat , 1984, Journal of Neuroscience Methods.
[41] R. Paro,et al. Homo‐ and heterodimerization of APP family members promotes intercellular adhesion , 2005, The EMBO journal.
[42] R. Tanzi,et al. Caspase activation increases beta-amyloid generation independently of caspase cleavage of the beta-amyloid precursor protein (APP). , 2003, The Journal of biological chemistry.
[43] E. Masliah,et al. Amyloid beta protein toxicity mediated by the formation of amyloid-beta protein precursor complexes. , 2003, Annals of neurology.
[44] S. Chandra,et al. A second cytotoxic proteolytic peptide derived from amyloid beta-protein precursor. , 2000, Nature medicine.
[45] B. Sommer,et al. Amyloid beta interacts with the amyloid precursor protein: a potential toxic mechanism in Alzheimer's disease. , 2000, Nature neuroscience.
[46] G. Robertson,et al. Involvement of caspases in proteolytic cleavage of Alzheimer's amyloid-beta precursor protein and amyloidogenic A beta peptide formation. , 1999, Cell.