A key role for the microglial NADPH oxidase in APP-dependent killing of neurons

[1]  P. Arthur,et al.  Role of NAD(P)H oxidase in the regulation of cardiac L-type Ca2+ channel function during acute hypoxia. , 2005, Cardiovascular research.

[2]  Deanna L. Taylor,et al.  Stimulation of Microglial Metabotropic Glutamate Receptor mGlu2 Triggers Tumor Necrosis Factor α-Induced Neurotoxicity in Concert with Microglial-Derived Fas Ligand , 2005, The Journal of Neuroscience.

[3]  J. D. McGaugh,et al.  Intraneuronal Aβ Causes the Onset of Early Alzheimer’s Disease-Related Cognitive Deficits in Transgenic Mice , 2005, Neuron.

[4]  K. Krause,et al.  Chemokine receptors in the central nervous system: role in brain inflammation and neurodegenerative diseases , 2005, Brain Research Reviews.

[5]  C. Haass,et al.  Amyloid β-induced Changes in Nitric Oxide Production and Mitochondrial Activity Lead to Apoptosis* , 2004, Journal of Biological Chemistry.

[6]  M. Bullido,et al.  Aβ production as consequence of cellular death of a human neuroblastoma overexpressing APP , 2004, FEBS letters.

[7]  R. Anwyl,et al.  β-Amyloid-Mediated Inhibition of NMDA Receptor-Dependent Long-Term Potentiation Induction Involves Activation of Microglia and Stimulation of Inducible Nitric Oxide Synthase and Superoxide , 2004, The Journal of Neuroscience.

[8]  J. Wegiel,et al.  Contribution of glial cells to the development of amyloid plaques in Alzheimer’s disease , 2004, Neurobiology of Aging.

[9]  Colin L. Masters,et al.  Neurodegenerative diseases and oxidative stress , 2004, Nature Reviews Drug Discovery.

[10]  M. Duchen,et al.  β-Amyloid Peptides Induce Mitochondrial Dysfunction and Oxidative Stress in Astrocytes and Death of Neurons through Activation of NADPH Oxidase , 2004, The Journal of Neuroscience.

[11]  K. Ishii,et al.  The LPS receptor (CD14) links innate immunity with Alzheimer's disease , 2004, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[12]  K. Krause,et al.  Chemokine-induced cell death in CCR5-expressing neuroblastoma cells , 2003, Journal of Neuroimmunology.

[13]  I. Nishimoto,et al.  Characterization of the toxic mechanism triggered by Alzheimer's amyloid‐β peptides via p75 neurotrophin receptor in neuronal hybrid cells , 2003, Journal of neuroscience research.

[14]  K. Krause,et al.  A Role for NOX NADPH Oxidases in Alzheimer's Disease and Other Types of Dementia? , 2003, IUBMB life.

[15]  James L. Buescher,et al.  Amyloid precursor protein‐processing products affect mononuclear phagocyte activation: pathways for sAPP‐ and Aβ‐mediated neurotoxicity , 2003 .

[16]  S. H. Kim,et al.  Brain-derived neurotrophic factor can act as a pronecrotic factor through transcriptional and translational activation of NADPH oxidase , 2002, The Journal of cell biology.

[17]  K. Krause,et al.  The HIV-1 Nef Protein and Phagocyte NADPH Oxidase Activation* , 2002, The Journal of Biological Chemistry.

[18]  P. Greengard,et al.  Intraneuronal Alzheimer abeta42 accumulates in multivesicular bodies and is associated with synaptic pathology. , 2002, The American journal of pathology.

[19]  R. Levy,et al.  Essential Requirement of Cytosolic Phospholipase A2for Stimulation of NADPH Oxidase-associated Diaphorase Activity in Granulocyte-like Cells* , 2001, The Journal of Biological Chemistry.

[20]  M. Smith,et al.  Activation of NADPH oxidase in Alzheimer's disease brains. , 2000, Biochemical and biophysical research communications.

[21]  P. Adlard,et al.  The cause of neuronal degeneration in Alzheimer's disease , 2000, Progress in Neurobiology.

[22]  S. Estus,et al.  t NADPH Oxidase Contributes Directly to Oxidative Stress and Apoptosis in Nerve Growth Factor-Deprived Sympathetic Neurons , 2000, The Journal of Neuroscience.

[23]  F. Rossi,et al.  beta-amyloid activates the O-2 forming NADPH oxidase in microglia, monocytes, and neutrophils. A possible inflammatory mechanism of neuronal damage in Alzheimer's disease. , 1999, The Journal of biological chemistry.

[24]  T. Hope,et al.  Woodchuck Hepatitis Virus Posttranscriptional Regulatory Element Enhances Expression of Transgenes Delivered by Retroviral Vectors , 1999, Journal of Virology.

[25]  W. Gong,et al.  A Seven-transmembrane, G Protein–coupled Receptor, FPRL1, Mediates the Chemotactic Activity of Serum Amyloid A for Human Phagocytic Cells , 1999, The Journal of experimental medicine.

[26]  J. Zweier,et al.  Measurement and characterization of superoxide generation in microglial cells: evidence for an NADPH oxidase-dependent pathway. , 1998, Archives of biochemistry and biophysics.

[27]  R. Levy,et al.  Essential Requirement of Cytosolic Phospholipase A2for Activation of the Phagocyte NADPH Oxidase* , 1998, The Journal of Biological Chemistry.

[28]  B. Sommer,et al.  Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[29]  J. Loike,et al.  Scavenger receptor-mediated adhesion of microglia to β-amyloid fibrils , 1996, Nature.

[30]  D. Ferrari,et al.  Activation of microglial cells by β-amyloid protein and interferon-γ , 1995, Nature.

[31]  S. Chanock,et al.  Gene targeting of X chromosome-linked chronic granulomatous disease locus in a human myeloid leukemia cell line and rescue by expression of recombinant gp91phox. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[32]  S. Younkin,et al.  Release of excess amyloid beta protein from a mutant amyloid beta protein precursor. , 1993, Science.

[33]  D. Selkoe,et al.  Mutation of the β-amyloid precursor protein in familial Alzheimer's disease increases β-protein production , 1992, Nature.

[34]  K. Yoshikawa,et al.  Degeneration in vitro of post-mitotic neurons overexpressing the Alzheimer amyloid protein precursor , 1992, Nature.

[35]  F. Bricaire,et al.  Neurodegenerative diseases and oxidative stress. , 2004, Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie.

[36]  J. Berman,et al.  CD36, a class B scavenger receptor, is expressed on microglia in Alzheimer's disease brains and can mediate production of reactive oxygen species in response to beta-amyloid fibrils. , 2002, The American journal of pathology.