Regulation of Tau Pathology by the Microglial Fractalkine Receptor

[1]  R. Ransohoff,et al.  CX3CR1 deficiency alters microglial activation and reduces beta-amyloid deposition in two Alzheimer's disease mouse models. , 2010, The American journal of pathology.

[2]  Richard M. Page,et al.  Microglial Cx3cr1 knockout prevents neuron loss in a mouse model of Alzheimer's disease , 2010, Nature Neuroscience.

[3]  K. Herrup,et al.  NSAIDs prevent, but do not reverse, neuronal cell cycle reentry in a mouse model of Alzheimer disease. , 2009, The Journal of clinical investigation.

[4]  A. Fagan,et al.  Multimodal techniques for diagnosis and prognosis of Alzheimer's disease , 2009, Nature.

[5]  W. Masocha.  Systemic lipopolysaccharide (LPS)-induced microglial activation results in different temporal reduction of CD200 and CD200 receptor gene expression in the brain , 2009, Journal of Neuroimmunology.

[6]  K. Herrup,et al.  The PI3K-Akt-mTOR pathway regulates Aβ oligomer induced neuronal cell cycle events , 2009, Molecular Neurodegeneration.

[7]  W. Noble,et al.  Minocycline reduces the development of abnormal tau species in models of Alzheimer's disease , 2009, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[8]  V. Perry,et al.  Systemic Inflammation Induces Acute Behavioral and Cognitive Changes and Accelerates Neurodegenerative Disease , 2009, Biological Psychiatry.

[9]  Z. Környei,et al.  Role of CX3CR1 (Fractalkine Receptor) in Brain Damage and Inflammation Induced by Focal Cerebral Ischemia in Mouse , 2008, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[10]  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.

[11]  W. Noble,et al.  Kinase activities increase during the development of tauopathy in htau mice , 2007, Journal of neurochemistry.

[12]  P. Debré,et al.  CX3CR1-dependent subretinal microglia cell accumulation is associated with cardinal features of age-related macular degeneration. , 2007, The Journal of clinical investigation.

[13]  J. Trojanowski,et al.  Synapse Loss and Microglial Activation Precede Tangles in a P301S Tauopathy Mouse Model , 2007, Neuron.

[14]  F. Crews,et al.  Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration , 2007, Glia.

[15]  P. Mantyh,et al.  Sensory neurons and their supporting cells located in the trigeminal, thoracic and lumbar ganglia differentially express markers of injury following intravenous administration of paclitaxel in the rat , 2006, Neuroscience Letters.

[16]  Steffen Jung,et al.  Control of microglial neurotoxicity by the fractalkine receptor , 2006, Nature Neuroscience.

[17]  Jason Eriksen,et al.  A decade of modeling Alzheimer's disease in transgenic mice. , 2006, Trends in genetics : TIG.

[18]  Alexander Gerhard,et al.  In vivo imaging of microglial activation with [11C](R)‐PK11195 PET in progressive supranuclear palsy , 2006, Movement disorders : official journal of the Movement Disorder Society.

[19]  V. Perry,et al.  Central and Systemic Endotoxin Challenges Exacerbate the Local Inflammatory Response and Increase Neuronal Death during Chronic Neurodegeneration , 2005, The Journal of Neuroscience.

[20]  F. LaFerla,et al.  Lipopolysaccharide-Induced Inflammation Exacerbates Tau Pathology by a Cyclin-Dependent Kinase 5-Mediated Pathway in a Transgenic Model of Alzheimer's Disease , 2005, The Journal of Neuroscience.

[21]  P. Hof,et al.  Cell-Cycle Reentry and Cell Death in Transgenic Mice Expressing Nonmutant Human Tau Isoforms , 2005, The Journal of Neuroscience.

[22]  R. Hughes.  The value of spontaneous alternation behavior (SAB) as a test of retention in pharmacological investigations of memory , 2004, Neuroscience & Biobehavioral Reviews.

[23]  L. Barbeito,et al.  Astrocytic nitric oxide triggers tau hyperphosphorylation in hippocampal neurons. , 2004, In vivo.

[24]  R. Maccioni,et al.  Interleukin-6 induces Alzheimer-type phosphorylation of tau protein by deregulating the cdk5/p35 pathway. , 2004, Experimental cell research.

[25]  J. Serratosa,et al.  High‐yield isolation of murine microglia by mild trypsinization , 2003, Glia.

[26]  A. Sun,et al.  P38 MAP kinase is activated at early stages in Alzheimer’s disease brain , 2003, Experimental Neurology.

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

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

[29]  A. Suzumura,et al.  Production and neuroprotective functions of fractalkine in the central nervous system , 2003, Brain Research.

[30]  S. Barger,et al.  Interleukin-1 Mediates Pathological Effects of Microglia on Tau Phosphorylation and on Synaptophysin Synthesis in Cortical Neurons through a p38-MAPK Pathway , 2003, The Journal of Neuroscience.

[31]  Xiongwei Zhu,et al.  The p38 pathway is activated in Pick disease and progressive supranuclear palsy: a mechanistic link between mitogenic pathways, oxidative stress, and tau , 2002, Neurobiology of Aging.

[32]  R. Mrak,et al.  Interleukin-1 promotion of MAPK-p38 overexpression in experimental animals and in Alzheimer's disease: potential significance for tau protein phosphorylation , 2001, Neurochemistry International.

[33]  P. Gebicke-haerter.  Microglia in neurodegeneration: Molecular aspects , 2001, Microscopy research and technique.

[34]  D. Dickson,et al.  Microglial Activation Parallels System Degeneration in Progressive Supranuclear Palsy and Corticobasal Degeneration , 2001, Journal of neuropathology and experimental neurology.

[35]  A. Sher,et al.  Analysis of Fractalkine Receptor CX3CR1 Function by Targeted Deletion and Green Fluorescent Protein Reporter Gene Insertion , 2000, Molecular and Cellular Biology.

[36]  B. Monks,et al.  Toll-like receptor 4 imparts ligand-specific recognition of bacterial lipopolysaccharide. , 2000, The Journal of clinical investigation.

[37]  W. Markesbery,et al.  p38 Kinase Is Activated in the Alzheimer's Disease Brain , 1999, Journal of neurochemistry.

[38]  R. Miller,et al.  Chemokines regulate hippocampal neuronal signaling and gp120 neurotoxicity. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[39]  W. Streit,et al.  Role for neuronally derived fractalkine in mediating interactions between neurons and CX3CR1-expressing microglia. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[40]  M. Stoeckel,et al.  Brain inflammatory response induced by intracerebroventricular infusion of lipopolysaccharide: an immunohistochemical study , 1998, Brain Research.

[41]  Philip R. Cohen,et al.  Phosphorylation of microtubule‐associated protein tau by stress‐activated protein kinases , 1997, FEBS letters.

[42]  Philip R. Cohen,et al.  SB 203580 is a specific inhibitor of a MAP kinase homologue which is stimulated by cellular stresses and interleukin‐1 , 1995, FEBS letters.

[43]  Jerry L. Adams,et al.  A protein kinase involved in the regulation of inflammatory cytokine biosynthesis , 1994, Nature.

[44]  L. Tsai,et al.  p35 is a neural-specific regulatory subunit of cyclin-dependent kinase 5 , 1994, Nature.

[45]  R. Aebersold,et al.  A brain-specific activator of cyclin-dependent kinase 5 , 1994, Nature.

[46]  P. Cohen,et al.  Inactivation of glycogen synthase kinase-3 beta by phosphorylation: new kinase connections in insulin and growth-factor signalling. , 1993, The Biochemical journal.

[47]  H. Braak,et al.  Demonstration of Amyloid Deposits and Neurofibrillary Changes in Whole Brain Sections , 1991, Brain pathology.

[48]  P. Davies,et al.  A preparation of Alzheimer paired helical filaments that displays distinct tau proteins by polyacrylamide gel electrophoresis. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[49]  R. Pawlinski,et al.  Morphology of reactive microglia in the injured cerebral cortex. Fractal analysis and complementary quantitative methods , 2001, Journal of neuroscience research.