SOD1 (Copper/Zinc Superoxide Dismutase) Deficiency Drives Amyloid β Protein Oligomerization and Memory Loss in Mouse Model of Alzheimer Disease*
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Takao Kaneko | Shigeo Murayama | Noriaki Kinoshita | T. Kaneko | S. Tahara | T. Shirasawa | Takahiko Shimizu | S. Murayama | K. Irie | K. Barnham | Shoichi Tahara | Kevin J Barnham | Kazuhiro Irie | Kazuma Murakami | Takahiko Shimizu | Takuji Shirasawa | H. Hatsuta | K. Murakami | Y. Noda | Hiroyuki Hatsuta | Yoshihiro Noda | Nakaba Murata | N. Kinoshita | Nakaba Murata
[1] G. Glenner,et al. Alzheimer's disease: initial report of the purification and characterization of a novel cerebrovascular amyloid protein. 1984. , 2012, Biochemical and biophysical research communications.
[2] T. Shirasawa,et al. Cytoplasmic superoxide causes bone fragility owing to low‐turnover osteoporosis and impaired collagen cross‐linking , 2011, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[3] W. Klein,et al. Intraneuronal amyloid β oligomers cause cell death via endoplasmic reticulum stress, endosomal/lysosomal leakage, and mitochondrial dysfunction in vivo , 2011, Journal of neuroscience research.
[4] T. Shirasawa,et al. Insulin receptor mutation results in insulin resistance and hyperinsulinemia but does not exacerbate Alzheimer's-like phenotypes in mice. , 2011, Biochemical and biophysical research communications.
[5] T. Shirasawa,et al. Superoxide dismutase deficiency enhances superoxide levels in brain tissues during oxygenation and hypoxia‐reoxygenation , 2011, Journal of neuroscience research.
[6] D. Loeffler,et al. Specificity and sensitivity of the Abeta oligomer ELISA , 2011, Journal of Neuroscience Methods.
[7] T. Tabira,et al. Apomorphine treatment in Alzheimer mice promoting amyloid‐β degradation , 2011, Annals of neurology.
[8] C. Lippa. Review of Issue: Alzheimer’s Caregiver’s and Internet-Based Support Services: Do They Work? , 2011 .
[9] M. Maeda,et al. Presenilin-2 Mutation Causes Early Amyloid Accumulation and Memory Impairment in a Transgenic Mouse Model of Alzheimer's Disease , 2010, Journal of biomedicine & biotechnology.
[10] T. Shirasawa,et al. Silymarin Attenuated the Amyloid β Plaque Burden and Improved Behavioral Abnormalities in an Alzheimer’s Disease Mouse Model , 2010, Bioscience, biotechnology, and biochemistry.
[11] T. Shirasawa,et al. Monoclonal antibody against the turn of the 42-residue amyloid β-protein at positions 22 and 23. , 2010, ACS chemical neuroscience.
[12] Christopher C. J. Miller,et al. Deficiency of the copper chaperone for superoxide dismutase increases amyloid-β production. , 2010, Journal of Alzheimer's disease : JAD.
[13] R. Ramasamy,et al. RAGE Modulates Hypoxia/Reoxygenation Injury in Adult Murine Cardiomyocytes via JNK and GSK-3β Signaling Pathways , 2010, PloS one.
[14] Rie Teraoka,et al. A Mouse Model of Amyloid β Oligomers: Their Contribution to Synaptic Alteration, Abnormal Tau Phosphorylation, Glial Activation, and Neuronal Loss In Vivo , 2010, The Journal of Neuroscience.
[15] S. Scheff,et al. Oxidative Stress in the Progression of Alzheimer Disease in the Frontal Cortex , 2010, Journal of neuropathology and experimental neurology.
[16] D. Teplow,et al. Structure-neurotoxicity relationships of amyloid β-protein oligomers , 2009, Neuroscience Research.
[17] Xiaomin Song,et al. Amyloid-β and tau synergistically impair the oxidative phosphorylation system in triple transgenic Alzheimer's disease mice , 2009, Proceedings of the National Academy of Sciences.
[18] Seongman Kang,et al. Intracellular amyloid beta interacts with SOD1 and impairs the enzymatic activity of SOD1: implications for the pathogenesis of amyotrophic lateral sclerosis , 2009, Experimental & Molecular Medicine.
[19] Y. Ikeda,et al. Skin atrophy in cytoplasmic SOD-deficient mice and its complete recovery using a vitamin C derivative. , 2009, Biochemical and biophysical research communications.
[20] D. Teplow,et al. Amyloid β-Protein Assembly and Alzheimer Disease* , 2009, Journal of Biological Chemistry.
[21] Weiming Xia,et al. A specific enzyme-linked immunosorbent assay for measuring beta-amyloid protein oligomers in human plasma and brain tissue of patients with Alzheimer disease. , 2009, Archives of neurology.
[22] Shaomin Li,et al. Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory , 2008, Nature Medicine.
[23] 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.
[24] P. Moreira,et al. Brain oxidative stress in a triple-transgenic mouse model of Alzheimer disease. , 2008, Free radical biology & medicine.
[25] C. B. Rickman,et al. Targeting age-related macular degeneration with Alzheimer’s disease based immunotherapies: Anti-amyloid-β antibody attenuates pathologies in an age-related macular degeneration mouse model , 2008, Vision Research.
[26] P. Mcgeer,et al. Inflammatory aspects of Alzheimer disease and other neurodegenerative disorders. , 2008, Journal of Alzheimer's disease : JAD.
[27] George Perry,et al. Oxidative stress and neurotoxicity. , 2008, Chemical research in toxicology.
[28] Roberto Cappai,et al. The redox chemistry of the Alzheimer's disease amyloid β peptide , 2007 .
[29] C. Masters,et al. Mitochondrial Oxidative Stress Causes Hyperphosphorylation of Tau , 2007, PloS one.
[30] L. Mucke,et al. Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model , 2007, Science.
[31] W. Klein,et al. Aβ Oligomers Induce Neuronal Oxidative Stress through an N-Methyl-D-aspartate Receptor-dependent Mechanism That Is Blocked by the Alzheimer Drug Memantine* , 2007, Journal of Biological Chemistry.
[32] H. Asao,et al. Elevated oxidative stress in erythrocytes due to a SOD1 deficiency causes anaemia and triggers autoantibody production. , 2007, The Biochemical journal.
[33] D. Selkoe,et al. Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptide , 2007, Nature Reviews Molecular Cell Biology.
[34] T. Shirasawa,et al. CuZn-SOD Deficiency Causes ApoB Degradation and Induces Hepatic Lipid Accumulation by Impaired Lipoprotein Secretion in Mice* , 2006, Journal of Biological Chemistry.
[35] Kei Shinoda,et al. Drusen, choroidal neovascularization, and retinal pigment epithelium dysfunction in SOD1-deficient mice: a model of age-related macular degeneration. , 2006, Proceedings of the National Academy of Sciences of the United States of America.
[36] L. Mucke,et al. Reduction in Mitochondrial Superoxide Dismutase Modulates Alzheimer's Disease-Like Pathology and Accelerates the Onset of Behavioral Changes in Human Amyloid Precursor Protein Transgenic Mice , 2006, The Journal of Neuroscience.
[37] Mark Bowlby,et al. Early-onset behavioral and synaptic deficits in a mouse model of Alzheimer's disease. , 2006, Proceedings of the National Academy of Sciences of the United States of America.
[38] R. Kayed,et al. Drusen deposits associated with aging and age-related macular degeneration contain nonfibrillar amyloid oligomers. , 2006, The Journal of clinical investigation.
[39] M. Nagao,et al. Formation and stabilization model of the 42-mer Abeta radical: implications for the long-lasting oxidative stress in Alzheimer's disease. , 2005, Journal of the American Chemical Society.
[40] S. Ichinose,et al. The potential role of amyloid beta in the pathogenesis of age-related macular degeneration. , 2005, The Journal of clinical investigation.
[41] George Perry,et al. Oxidative Stress and Neurodegeneration , 2005, Annals of the New York Academy of Sciences.
[42] K. Freeman,et al. BACE1 Cytoplasmic Domain Interacts with the Copper Chaperone for Superoxide Dismutase-1 and Binds Copper* , 2005, Journal of Biological Chemistry.
[43] M A Lovell,et al. Increased oxidative damage in nuclear and mitochondrial DNA in Alzheimer's disease , 2005, Journal of neurochemistry.
[44] Gang-yi Wu,et al. Synaptic localization of a functional NADPH oxidase in the mouse hippocampus , 2005, Molecular and Cellular Neuroscience.
[45] Ian Parker,et al. Calcium Dysregulation and Membrane Disruption as a Ubiquitous Neurotoxic Mechanism of Soluble Amyloid Oligomers*♦ , 2005, Journal of Biological Chemistry.
[46] S. Murayama,et al. Neuropathological diagnostic criteria for Alzheimer's disease , 2004, Neuropathology : official journal of the Japanese Society of Neuropathology.
[47] C. Masters,et al. Tyrosine gated electron transfer is key to the toxic mechanism of Alzheimer's disease β‐amyloid , 2004, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[48] T. Kaneko,et al. Suppression of 8-Oxo-2′-deoxyguanosine Formation and Carcinogenesis Induced by N-Nitrosobis(2-oxopropyl)amine in Hamsters by Esculetin and Esculin , 2004, Free radical research.
[49] William M. Mauck,et al. Increased plaque burden in brains of APP mutant MnSOD heterozygous knockout mice , 2004, Journal of neurochemistry.
[50] Colin L. Masters,et al. Neurodegenerative diseases and oxidative stress , 2004, Nature Reviews Drug Discovery.
[51] C. Duyckaerts,et al. Escourolle and Poirier's Manual of Basic Neuropathology , 2004 .
[52] T. Bayer,et al. Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Aβ production in APP23 transgenic mice , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[53] Carl W. Cotman,et al. Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of Pathogenesis , 2003, Science.
[54] Alexander J. Rivest,et al. The Alzheimer's Aβ-peptide is deposited at sites of complement activation in pathologic deposits associated with aging and age-related macular degeneration , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[55] W. K. Cullen,et al. Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo , 2002, Nature.
[56] D. Harman. Alzheimer's Disease: Role of Aging in Pathogenesis , 2002, Annals of the New York Academy of Sciences.
[57] I. Fridovich,et al. Subcellular Distribution of Superoxide Dismutases (SOD) in Rat Liver , 2001, The Journal of Biological Chemistry.
[58] George A. Carlson,et al. Exogenous Aβ1–40 Reproduces Cerebrovascular Alterations Resulting from Amyloid Precursor Protein Overexpression in Mice , 2000, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[59] 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.
[60] D. Butterfield,et al. Review: Alzheimer's amyloid beta-peptide-associated free radical oxidative stress and neurotoxicity. , 2000, Journal of structural biology.
[61] D. Borchelt,et al. SOD1 rescues cerebral endothelial dysfunction in mice overexpressing amyloid precursor protein , 1999, Nature Neuroscience.
[62] S. Younkin,et al. Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice , 1996, Science.
[63] J. Piatigorsky,et al. Oxidative Stress Increases Production of -Amyloid Precursor Protein and -Amyloid (A) in Mammalian Lenses, and A Has Toxic Effects on Lens Epithelial Cells (*) , 1996, The Journal of Biological Chemistry.
[64] K. Jellinger,et al. Decreased Catalase Activity but Unchanged Superoxide Dismutase Activity in Brains of Patients with Dementia of Alzheimer Type , 1995, Journal of neurochemistry.
[65] J. Richardson. Free Radicals in the Genesis of Alzheimer's Disease a , 1993, Annals of the New York Academy of Sciences.
[66] John Q. Trojanowski,et al. Abnormal tau phosphorylation at Ser396 in alzheimer's disease recapitulates development and contributes to reduced microtubule binding , 1993, Neuron.
[67] C. Masters,et al. Amyloid plaque core protein in Alzheimer disease and Down syndrome. , 1985, Proceedings of the National Academy of Sciences of the United States of America.
[68] B. Winblad,et al. Superoxide dismutase isoenzymes in normal brains and in brains from patients with dementia of Alzheimer type , 1985, Journal of the Neurological Sciences.