AGEs/RAGE complex upregulates BACE1 via NF-κB pathway activation

[1]  G. McKhann,et al.  RAGE-mediated signaling contributes to intraneuronal transport of amyloid-β and neuronal dysfunction , 2009, Proceedings of the National Academy of Sciences.

[2]  I. Mook‐Jung,et al.  RAGE regulates BACE1 and Aβ generation via NFAT1 activation in Alzheimer's disease animal model , 2009, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[3]  M. Tabaton,et al.  The up‐regulation of BACE1 mediated by hypoxia and ischemic injury: role of oxidative stress and HIF1α , 2009, Journal of neurochemistry.

[4]  A. Richardson,et al.  Lipid peroxidation up‐regulates BACE1 expression in vivo: a possible early event of amyloidogenesis in Alzheimer’s disease , 2008, Journal of neurochemistry.

[5]  G. Dawson,et al.  Expression of the receptor for advanced glycation end products in oligodendrocytes in response to oxidative stress , 2008, Journal of neuroscience research.

[6]  J. Forbes,et al.  Advanced glycation: implications in tissue damage and disease. , 2008, Protein and peptide letters.

[7]  F. Checler,et al.  NFκB-dependent Control of BACE1 Promoter Transactivation by Aβ42* , 2008, Journal of Biological Chemistry.

[8]  Su-Yen Goh,et al.  The role of advanced glycation end products in progression and complications of diabetes , 2008 .

[9]  M. Mattson,et al.  Oxidative stress activates a positive feedback between the γ‐ and β‐secretase cleavages of the β‐amyloid precursor protein , 2007 .

[10]  M. Tabaton,et al.  The increased activity of BACE1 correlates with oxidative stress in Alzheimer's disease , 2007, Neurobiology of Aging.

[11]  Paul J Thornalley,et al.  Advanced glycation endproducts: what is their relevance to diabetic complications? , 2007, Diabetes, obesity & metabolism.

[12]  G. Münch,et al.  Coffee and Maillard products activate NF-kappaB in macrophages via H2O2 production. , 2007, Molecular nutrition & food research.

[13]  Gang Xiao,et al.  Membrane-mediated Amyloidogenesis and the Promotion of Oxidative Lipid Damage by Amyloid β Proteins* , 2007, Journal of Biological Chemistry.

[14]  T. Arendt,et al.  Effect of Pseudophosphorylation and Cross-linking by Lipid Peroxidation and Advanced Glycation End Product Precursors on Tau Aggregation and Filament Formation* , 2007, Journal of Biological Chemistry.

[15]  F. Hayase,et al.  Detection and Determination of Glyceraldehyde-Derived Pyridinium-Type Advanced Glycation End Product in Streptozotocin-Induced Diabetic Rats , 2007, Bioscience, biotechnology, and biochemistry.

[16]  F. Hayase,et al.  Chemistry and Biological Effects of Melanoidins and Glyceraldehyde‐Derived Pyridinium as Advanced Glycation End Products , 2005, Annals of the New York Academy of Sciences.

[17]  H. Qing,et al.  Oxidative stress potentiates BACE1 gene expression and Aβ generation , 2005, Journal of Neural Transmission.

[18]  G. Perry,et al.  β‐Site APP cleaving enzyme up‐regulation induced by 4‐hydroxynonenal is mediated by stress‐activated protein kinases pathways , 2005, Journal of neurochemistry.

[19]  K. Safranow,et al.  A sensitive and specific HPLC method for the determination of total pentosidine concentration in plasma. , 2004, Journal of biochemical and biophysical methods.

[20]  Xi Chen,et al.  RAGE potentiates Aβ‐induced perturbation of neuronal function in transgenic mice , 2004, The EMBO journal.

[21]  M. Mattson Pathways towards and away from Alzheimer's disease , 2004, Nature.

[22]  Xiongwei Zhu,et al.  Alzheimer's disease: the two-hit hypothesis , 2004, The Lancet Neurology.

[23]  L. Tsai,et al.  BACE1 Suppression by RNA Interference in Primary Cortical Neurons* , 2004, Journal of Biological Chemistry.

[24]  G. Jerums,et al.  Evolving concepts in advanced glycation, diabetic nephropathy, and diabetic vascular disease. , 2003, Archives of biochemistry and biophysics.

[25]  R. Martins,et al.  Amyloid-β: a chameleon walking in two worlds: a review of the trophic and toxic properties of amyloid-β , 2003, Brain Research Reviews.

[26]  G. Robino,et al.  H2o2 and 4-hydroxynonenal mediate amyloid β-induced neuronal apoptosis by activating jnks and p38mapk , 2003, Experimental Neurology.

[27]  G. Perry,et al.  Oxidative Stress Increases Expression and Activity of BACE in NT2 Neurons , 2002, Neurobiology of Disease.

[28]  A. Schmidt,et al.  The multiligand receptor RAGE as a progression factor amplifying immune and inflammatory responses. , 2001, The Journal of clinical investigation.

[29]  L. Lue,et al.  Involvement of Microglial Receptor for Advanced Glycation Endproducts (RAGE) in Alzheimer's Disease: Identification of a Cellular Activation Mechanism , 2001, Experimental Neurology.

[30]  Z. Makita,et al.  Alternative routes for the formation of immunochemically distinct advanced glycation end-products in vivo. , 2001, Current molecular medicine.

[31]  D. Selkoe Alzheimer's disease: genes, proteins, and therapy. , 2001, Physiological reviews.

[32]  P. Riederer,et al.  Transition metal-mediated glycoxidation accelerates cross-linking of beta-amyloid peptide. , 2000, European journal of biochemistry.

[33]  Y. Ihara,et al.  Oxidative stress induces intracellular accumulation of amyloid beta-protein (Abeta) in human neuroblastoma cells. , 2000, Biochemistry.

[34]  M. Tabaton,et al.  Oxidative Stress Induces Increase in Intracellular Amyloid β-Protein Production and Selective Activation of βI and βII PKCs in NT2 Cells , 2000 .

[35]  A. Schmidt,et al.  Activation of receptor for advanced glycation end products: a mechanism for chronic vascular dysfunction in diabetic vasculopathy and atherosclerosis. , 1999, Circulation research.

[36]  Z. Makita,et al.  Advanced glycation end products in Alzheimer's disease and other neurodegenerative diseases. , 1998, The American journal of pathology.

[37]  H. James,et al.  The generation of superoxide anions in glycation reactions with sugars, osones, and 3-deoxyosones. , 1998, Biochemical and biophysical research communications.

[38]  R. Shenkar,et al.  Hemorrhage Activates Myocardial NF?B and Increases TNF-a in the Heart , 1997 .

[39]  A. Schmidt,et al.  Activation of the Receptor for Advanced Glycation End Products Triggers a p21 ras -dependent Mitogen-activated Protein Kinase Pathway Regulated by Oxidant Stress* , 1997, The Journal of Biological Chemistry.

[40]  X. Chen,et al.  RAGE and amyloid-β peptide neurotoxicity in Alzheimer's disease , 1996, Nature.

[41]  J. Zweier,et al.  Non-enzymatically glycated tau in Alzheimer's disease induces neuronal oxidant stress resulting in cytokine gene expression and release of amyloid β-peptide , 1995, Nature Medicine.

[42]  Q. Pye,et al.  Cytotoxic effects of autoxidative glycation. , 1995, Free radical biology & medicine.

[43]  J. Ávila,et al.  Analysis of microtubule-associated protein tau glycation in paired helical filaments. , 1994, The Journal of biological chemistry.

[44]  C. W. Scott,et al.  Glycated tau protein in Alzheimer disease: a mechanism for induction of oxidant stress. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[45]  M. Smith,et al.  Advanced Maillard reaction end products are associated with Alzheimer disease pathology , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[46]  R. Bucala,et al.  Advanced glycation end products contribute to amyloidosis in Alzheimer disease. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[47]  F. Zoccarato,et al.  Identification of an NADH plus iron dependent, Ca2+ activated hydrogen peroxide production in synaptosomes. , 1993, Biochimica et biophysica acta.

[48]  W. Hurley,et al.  Isolation and characterization of two binding proteins for advanced glycosylation end products from bovine lung which are present on the endothelial cell surface. , 1992, The Journal of biological chemistry.

[49]  K. O. Elliston,et al.  Cloning and expression of a cell surface receptor for advanced glycosylation end products of proteins. , 1992, The Journal of biological chemistry.

[50]  M. Brownlee,et al.  Free radical generation by early glycation products: a mechanism for accelerated atherogenesis in diabetes. , 1990, Biochemical and biophysical research communications.

[51]  A. Cerami,et al.  Advanced products of nonenzymatic glycosylation and the pathogenesis of diabetic vascular disease. , 1988, Diabetes/metabolism reviews.

[52]  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.

[53]  R. Belcher,et al.  A COLORIMETRIC MICRO-METHOD FOR THE DETERMINATION OF GLUTATHIONE. , 1965, The Biochemical journal.

[54]  G. van Dijk,et al.  Inflammation and NF-kappaB in Alzheimer's disease and diabetes. , 2009, Journal of Alzheimer's disease : JAD.

[55]  Allan Jones,et al.  Common pathological processes and transcriptional pathways in Alzheimer's disease and type 2 diabetes. , 2009, Journal of Alzheimer's disease : JAD.

[56]  S. Yamagishi,et al.  Involvement of toxic AGEs (TAGE) in the pathogenesis of diabetic vascular complications and Alzheimer's disease. , 2009, Journal of Alzheimer's disease : JAD.

[57]  E. Kojro,et al.  Regulated proteolysis of RAGE and AbetaPP as possible link between type 2 diabetes mellitus and Alzheimer's disease. , 2009, Journal of Alzheimer's disease : JAD.

[58]  George Perry,et al.  Oxidative stress in diabetes and Alzheimer's disease. , 2009, Journal of Alzheimer's disease : JAD.

[59]  J. Blass The up-regulation of BACE1 mediated by hypoxia and ischemic injury: role of oxidative stress and HIF1alpha , 2009 .

[60]  M. Mattson,et al.  Oxidative stress activates a positive feedback between the gamma- and beta-secretase cleavages of the beta-amyloid precursor protein. , 2008, Journal of neurochemistry.

[61]  S. Yamagishi,et al.  Diagnostic utility of serum or cerebrospinal fluid levels of toxic advanced glycation end-products (TAGE) in early detection of Alzheimer's disease. , 2007, Medical hypotheses.

[62]  S. Hoyer,et al.  Central insulin resistance as a trigger for sporadic Alzheimer-like pathology: an experimental approach. , 2007, Journal of neural transmission. Supplementum.

[63]  G. Münch,et al.  Coffee and Maillard products activate NF-kappaB in macrophages via H2O2 production. , 2007, Molecular nutrition & food research.

[64]  Peter Riederer,et al.  AGES in brain ageing: AGE-inhibitors as neuroprotective and anti-dementia drugs? , 2004, Biogerontology.

[65]  G. Perry,et al.  Amyloid-beta: a chameleon walking in two worlds: a review of the trophic and toxic properties of amyloid-beta. , 2003, Brain research. Brain research reviews.

[66]  R. Gonthier,et al.  Serum pentosidine as an indicator of Alzheimer's disease. , 2002, Journal of Alzheimer's disease : JAD.

[67]  M. Tabaton,et al.  Oxidative stress induces increase in intracellular amyloid beta-protein production and selective activation of betaI and betaII PKCs in NT2 cells. , 2000, Biochemical and biophysical research communications.

[68]  T. Harkany,et al.  Mechanisms of ß-Amyloid Neurotoxicity: Perspectives of Pharmacotherapy , 2000, Reviews in the neurosciences.

[69]  R. Shenkar,et al.  Hemorrhage activates myocardial NFkappaB and increases TNF-alpha in the heart. , 1997, Journal of molecular and cellular cardiology.

[70]  A. Schmidt,et al.  RAGE and amyloid-beta peptide neurotoxicity in Alzheimer's disease. , 1996, Nature.

[71]  R. Bucala,et al.  Advanced glycosylation: chemistry, biology, and implications for diabetes and aging. , 1992, Advances in pharmacology.

[72]  L. Flohé,et al.  Assays of glutathione peroxidase. , 1984, Methods in enzymology.

[73]  H. Aebi,et al.  Catalase in vitro. , 1984, Methods in enzymology.