Deletion of the type-1 interferon receptor in APPSWE/PS1ΔE9 mice preserves cognitive function and alters glial phenotype

[1]  S. Shultz,et al.  Deletion of the type-1 interferon receptor in APPSWE/PS1ΔE9 mice preserves cognitive function and alters glial phenotype , 2016, Acta Neuropathologica Communications.

[2]  I. Buers,et al.  Novel interferonopathies associated with mutations in RIG-I like receptors. , 2016, Cytokine & growth factor reviews.

[3]  M. Schwartz,et al.  Type I/II Interferon Balance in the Regulation of Brain Physiology and Pathology. , 2016, Trends in immunology.

[4]  David K. Wright,et al.  Ablation of Type-1 IFN Signaling in Hematopoietic Cells Confers Protection Following Traumatic Brain Injury , 2016, eNeuro.

[5]  Juliet M. Taylor,et al.  The contribution of neuroinflammation to amyloid toxicity in Alzheimer's disease , 2016, Journal of neurochemistry.

[6]  K. Garcia,et al.  Alpha and Beta Type 1 Interferon Signaling: Passage for Diverse Biologic Outcomes , 2016, Cell.

[7]  M. Schwartz,et al.  Breaking immune tolerance by targeting Foxp3+ regulatory T cells mitigates Alzheimer's disease pathology , 2015, Nature Communications.

[8]  G. Réus,et al.  The role of inflammation and microglial activation in the pathophysiology of psychiatric disorders , 2015, Neuroscience.

[9]  W. Klunk,et al.  Endogenous murine Aβ increases amyloid deposition in APP23 but not in APPPS1 transgenic mice , 2015, Neurobiology of Aging.

[10]  O. Garaschuk,et al.  Neuroinflammation in Alzheimer's disease , 2015, The Lancet Neurology.

[11]  A. Oxenius,et al.  Regulation of antiviral T cell responses by type I interferons , 2015, Nature Reviews Immunology.

[12]  M. Guillot-Sestier,et al.  Il10 Deficiency Rebalances Innate Immunity to Mitigate Alzheimer-Like Pathology , 2015, Neuron.

[13]  Nathan D. Price,et al.  IL-10 Alters Immunoproteostasis in APP Mice, Increasing Plaque Burden and Worsening Cognitive Behavior , 2015, Neuron.

[14]  A. Bowie,et al.  DNA sensors are expressed in astrocytes and microglia in vitro and are upregulated during gliosis in neurodegenerative disease , 2015, Glia.

[15]  I. Amit,et al.  Aging-induced type I interferon response at the choroid plexus negatively affects brain function , 2014, Science.

[16]  B. Vissel,et al.  Inconsistencies and Controversies Surrounding the Amyloid Hypothesis of Alzheimer's Disease , 2014, Acta neuropathologica communications.

[17]  L. Tan,et al.  Amyloid-β induces NLRP1-dependent neuronal pyroptosis in models of Alzheimer's disease , 2014, Cell Death and Disease.

[18]  J. Cirrito,et al.  Genetic Modulation of Soluble Aβ Rescues Cognitive and Synaptic Impairment in a Mouse Model of Alzheimer's Disease , 2014, The Journal of Neuroscience.

[19]  P. Adlard,et al.  Type-1 interferon signaling mediates neuro-inflammatory events in models of Alzheimer's disease , 2014, Neurobiology of Aging.

[20]  T. Owens,et al.  Interferons in the central nervous system: A few instruments play many tunes , 2014, Glia.

[21]  L. Ivashkiv,et al.  Regulation of type I interferon responses , 2013, Nature Reviews Immunology.

[22]  F. Heppner,et al.  Microglia actions in Alzheimer’s disease , 2013, Acta Neuropathologica.

[23]  P. Mcgeer,et al.  The amyloid cascade-inflammatory hypothesis of Alzheimer disease: implications for therapy , 2013, Acta Neuropathologica.

[24]  M. Heneka,et al.  NLRP3 is activated in Alzheimer´s disease and contributes to pathology in APP/PS1 mice , 2012, Nature.

[25]  York Winter,et al.  Inhibition of IL-12/IL-23 signaling reduces Alzheimer's disease–like pathology and cognitive decline , 2012, Nature Medicine.

[26]  T. Golde,et al.  Hippocampal expression of murine IL-4 results in exacerbation of amyloid deposition , 2012, Molecular Neurodegeneration.

[27]  K. Ozato,et al.  IRF8 Is a Critical Transcription Factor for Transforming Microglia into a Reactive Phenotype , 2012, Cell reports.

[28]  R. Myers,et al.  IκB kinase ε (IKKε) regulates the balance between type I and type II interferon responses , 2011, Proceedings of the National Academy of Sciences.

[29]  Yu Deng,et al.  Morris Water Maze Test for Learning and Memory Deficits in Alzheimer's Disease Model Mice , 2011, Journal of visualized experiments : JoVE.

[30]  Jean-Philippe Michaud,et al.  MyD88-adaptor protein acts as a preventive mechanism for memory deficits in a mouse model of Alzheimer's disease , 2011, Molecular Neurodegeneration.

[31]  Tsuyoshi Miyakawa,et al.  Dissection of Hippocampal Dentate Gyrus from Adult Mouse , 2009, Journal of visualized experiments : JoVE.

[32]  T. Suuronen,et al.  Inflammation in Alzheimer's disease: Amyloid-β oligomers trigger innate immunity defence via pattern recognition receptors , 2009, Progress in Neurobiology.

[33]  C. Masters,et al.  Increasing Cu bioavailability inhibits Aβ oligomers and tau phosphorylation , 2009, Proceedings of the National Academy of Sciences.

[34]  C. Masters,et al.  Increasing Cu bioavailability inhibits A beta oligomers and tau phosphorylation , 2009 .

[35]  T. Suuronen,et al.  Amyloid-β oligomers set fire to inflammasomes and induce Alzheimer's pathology , 2008, Journal of cellular and molecular medicine.

[36]  C. Masters,et al.  Rapid Restoration of Cognition in Alzheimer's Transgenic Mice with 8-Hydroxy Quinoline Analogs Is Associated with Decreased Interstitial Aβ , 2008, Neuron.

[37]  Michael W Parker,et al.  Crystallization and preliminary X-ray diffraction analysis of the Fab fragment of WO2, an antibody specific for the Abeta peptides associated with Alzheimer's disease. , 2008, Acta crystallographica. Section F, Structural biology and crystallization communications.

[38]  Paul J. Hertzog,et al.  Type I Interferon Receptors: Biochemistry and Biological Functions* , 2007, Journal of Biological Chemistry.

[39]  T. Maniatis,et al.  Multiple Functions of the IKK-Related Kinase IKKε in Interferon-Mediated Antiviral Immunity , 2007, Science.

[40]  T. Maniatis,et al.  Multiple functions of the IKK-related kinase IKKepsilon in interferon-mediated antiviral immunity. , 2007, Science.

[41]  P. Crack,et al.  Glutathione peroxidase 1 and a high cellular glutathione concentration are essential for effective organic hydroperoxide detoxification in astrocytes , 2006, Glia.

[42]  D. Barnes,et al.  Mutations in the gene encoding the 3′-5′ DNA exonuclease TREX1 cause Aicardi-Goutières syndrome at the AGS1 locus , 2006, Nature Genetics.

[43]  C. Ponting,et al.  Mutations in genes encoding ribonuclease H2 subunits cause Aicardi-Goutières syndrome and mimic congenital viral brain infection , 2006, Nature Genetics.

[44]  Shizuo Akira,et al.  Innate immune recognition of viral infection , 2006, Nature Immunology.

[45]  F. Mégret,et al.  Monique Lafon Producers of Beta Interferon Human Neurons to Become Strong Virus Infection Switches Tlr-3-positive , 2005 .

[46]  T. Arendt,et al.  Methylglyoxal, Glyoxal, and Their Detoxification in Alzheimer's Disease , 2005, Annals of the New York Academy of Sciences.

[47]  K. Conzelmann.  Transcriptional Activation of Alpha/Beta Interferon Genes: Interference by Nonsegmented Negative-Strand RNA Viruses , 2005, Journal of Virology.

[48]  Hideo Negishi,et al.  IRF-7 is the master regulator of type-I interferon-dependent immune responses , 2005, Nature.

[49]  P. Hertzog,et al.  Diminished Akt phosphorylation in neurons lacking glutathione peroxidase‐1 (Gpx1) leads to increased susceptibility to oxidative stress‐induced cell death , 2005, Journal of neurochemistry.

[50]  T. Arendt,et al.  Age- and stage-dependent accumulation of advanced glycation end products in intracellular deposits in normal and Alzheimer's disease brains. , 2004, Cerebral cortex.

[51]  D. Borchelt,et al.  APP processing and amyloid deposition in mice haplo-insufficient for presenilin 1 , 2004, Neurobiology of Aging.

[52]  T. Suzutani,et al.  Induction of Suppressor of Cytokine Signaling-3 by Herpes Simplex Virus Type 1 Contributes to Inhibition of the Interferon Signaling Pathway , 2004, Journal of Virology.

[53]  Joanna L. Jankowsky,et al.  Mutant presenilins specifically elevate the levels of the 42 residue β-amyloid peptide in vivo: evidence for augmentation of a 42-specific γ secretase , 2004 .

[54]  D. Borchelt,et al.  Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase. , 2004, Human molecular genetics.

[55]  C. Masters,et al.  Neurotoxic, Redox-competent Alzheimer's β-Amyloid Is Released from Lipid Membrane by Methionine Oxidation* , 2003, Journal of Biological Chemistry.

[56]  Thomas Klockgether,et al.  Nonsteroidal Anti-Inflammatory Drugs and Peroxisome Proliferator-Activated Receptor-γ Agonists Modulate Immunostimulated Processing of Amyloid Precursor Protein through Regulation of β-Secretase , 2003, The Journal of Neuroscience.

[57]  K. Honda,et al.  Essential role of IRF-3 in lipopolysaccharide-induced interferon-beta gene expression and endotoxin shock. , 2003, Biochemical and biophysical research communications.

[58]  Michael T Heneka,et al.  Nonsteroidal anti-inflammatory drugs and peroxisome proliferator-activated receptor-gamma agonists modulate immunostimulated processing of amyloid precursor protein through regulation of beta-secretase. , 2003, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[59]  T. Arendt,et al.  Aberrant expression of NOS isoforms in Alzheimer’s disease is structurally related to nitrotyrosine formation , 2002, Brain Research.

[60]  Thomas D. Schmittgen,et al.  Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. , 2001, Methods.

[61]  Rong Wang,et al.  A subset of NSAIDs lower amyloidogenic Aβ42 independently of cyclooxygenase activity , 2001, Nature.

[62]  D. Selkoe.  Alzheimer's disease results from the cerebral accumulation and cytotoxicity of amyloid beta-protein. , 2001, Journal of Alzheimer's disease : JAD.

[63]  P. Mcgeer,et al.  Autotoxicity and Alzheimer disease. , 2000, Archives of neurology.

[64]  P. Mcgeer,et al.  Alzheimer disease and neuroinflammation. , 2000, Journal of neural transmission. Supplementum.

[65]  P. Riederer,et al.  Free radicals in Alzheimer's disease. , 1998, Journal of neural transmission. Supplementum.

[66]  P. Riederer,et al.  Alzheimer's disease – synergistic effects of glucose deficit, oxidative stress and advanced glycation endproducts , 1998, Journal of Neural Transmission.

[67]  Warren S. Alexander,et al.  A family of cytokine-inducible inhibitors of signalling , 1997, Nature.

[68]  J. Breitner.  The role of anti-inflammatory drugs in the prevention and treatment of Alzheimer's disease. , 1996, Annual review of medicine.

[69]  M. Tymms,et al.  A null mutation in the gene encoding a type I interferon receptor component eliminates antiproliferative and antiviral responses to interferons alpha and beta and alters macrophage responses. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[70]  P. Chomczyński,et al.  A reagent for the single-step simultaneous isolation of RNA, DNA and proteins from cell and tissue samples. , 1993, BioTechniques.

[71]  J. McCubrey,et al.  Use of an aqueous soluble tetrazolium/formazan assay to measure viability and proliferation of lymphokine-dependent cell lines. , 1993, Journal of immunological methods.

[72]  H. Wiśniewski,et al.  Abnormal phosphorylation of the microtubule-associated protein tau (tau) in Alzheimer cytoskeletal pathology. , 1986, Proceedings of the National Academy of Sciences of the United States of America.

[73]  M. M. Bradford.  A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. , 1976, Analytical biochemistry.