Role of oxidative stress on β-amyloid neurotoxicity elicited during impairment of energy metabolism in the hippocampus: Protection by antioxidants

[1]  L. Massieu,et al.  Disruption of endoplasmic reticulum calcium stores is involved in neuronal death induced by glycolysis inhibition in cultured hippocampal neurons , 2005, Journal of neuroscience research.

[2]  Roger Kurlan,et al.  A focus on the synapse for neuroprotection in Alzheimer disease and other dementias , 2004, Neurology.

[3]  D. Butterfield,et al.  Amyloid β‐Peptide(1‐42) Contributes to the Oxidative Stress and Neurodegeneration Found in Alzheimer Disease Brain , 2004, Brain pathology.

[4]  D. Foley,et al.  Midlife dietary intake of antioxidants and risk of late-life incident dementia: the Honolulu-Asia Aging Study. , 2004, American journal of epidemiology.

[5]  D. Butterfield,et al.  Alzheimer’s amyloid β-peptide (1–42): involvement of methionine residue 35 in the oxidative stress and neurotoxicity properties of this peptide , 2004, Neurobiology of Aging.

[6]  Thomas Wisniewski,et al.  Amyloid‐β Deposition Is Associated with Decreased Hippocampal Glucose Metabolism and Spatial Memory Impairment in APP/PS1 Mice , 2004 .

[7]  J. Trojanowski,et al.  Early Vitamin E supplementation in young but not aged mice reduces Aβ levels and amyloid deposition in a transgenic model of Alzheimer's disease , 2004, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[8]  L. Massieu,et al.  Acetoacetate protects hippocampal neurons against glutamate-mediated neuronal damage during glycolysis inhibition , 2003, Neuroscience.

[9]  T. Ueda,et al.  Glycolysis and Glutamate Accumulation into Synaptic Vesicles , 2003, The Journal of Biological Chemistry.

[10]  W. T. Lee,et al.  The mechanisms of neuronal death produced by mitochondrial toxin 3-nitropropionic acid: the roles of N-methyl-D-aspartate glutamate receptors and mitochondrial calcium overload , 2002, Neuroscience.

[11]  G. Kim,et al.  Involvement of Superoxide in Excitotoxicity and DNA Fragmentation in Striatal Vulnerability in Mice after Treatment with the Mitochondrial Toxin, 3-Nitropropionic Acid , 2002, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[12]  C. Arias,et al.  β-Amyloid Neurotoxicity Is Exacerbated during Glycolysis Inhibition and Mitochondrial Impairment in the Rat Hippocampus in Vivo and in Isolated Nerve Terminals: Implications for Alzheimer's Disease , 2002, Experimental Neurology.

[13]  C. Lauderback,et al.  Lipid peroxidation and protein oxidation in Alzheimer's disease brain: Potential causes and consequences involving amyloid β-peptide-associated free radical oxidative stress , 2002 .

[14]  C. Arias,et al.  β‐Amyloid peptide induces ultrastructural changes in synaptosomes and potentiates mitochondrial dysfunction in the presence of ryanodine , 2002, Journal of neuroscience research.

[15]  G. M. Cole,et al.  Phenolic anti-inflammatory antioxidant reversal of Aβ-induced cognitive deficits and neuropathology , 2001, Neurobiology of Aging.

[16]  L. Massieu,et al.  Neurotoxicity of glutamate uptake inhibition in vivo: correlation with succinate dehydrogenase activity and prevention by energy substrates , 2001, Neuroscience.

[17]  Jean-Marie Annoni,et al.  Brain energy metabolism in Alzheimer’s disease: 99mTc-HMPAO SPECT imaging during verbal fluency and role of astrocytes in the cellular mechanism of 99mTc-HMPAO retention , 2001, Brain Research Reviews.

[18]  S. Davis,et al.  Generation of Aggregated β-Amyloid in the Rat Hippocampus Impairs Synaptic Transmission and Plasticity and Causes Memory Deficits , 2001, The Journal of Neuroscience.

[19]  Virginia M. Y. Lee,et al.  Increased Lipid Peroxidation Precedes Amyloid Plaque Formation in an Animal Model of Alzheimer Amyloidosis , 2001, The Journal of Neuroscience.

[20]  G. Reiser,et al.  Requirement of glycolytic and mitochondrial energy supply for loading of Ca2+ stores and InsP3‐mediated Ca2+ signaling in rat hippocampus astrocytes , 2000, Journal of neuroscience research.

[21]  V. Haroutunian,et al.  CNS oxidative stress associated with the kainic acid rodent model of experimental epilepsy , 2000, Epilepsy Research.

[22]  R. Floyd.  Antioxidants, oxidative stress, and degenerative neurological disorders. , 1999, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.

[23]  Xin Eric Wang,et al.  Vitamin E and its function in membranes. , 1999, Progress in lipid research.

[24]  D. Butterfield,et al.  In vitro and in vivo oxidative stress associated with Alzheimer's amyloid beta-peptide (1-42) , 1999, Neurobiology of aging.

[25]  R. Nicoll,et al.  Plaque-independent disruption of neural circuits in Alzheimer's disease mouse models. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[26]  C. Behl.  Alzheimer's disease and oxidative stress: implications for novel therapeutic approaches , 1999, Progress in Neurobiology.

[27]  T. Kameyama,et al.  Protective effects of idebenone and α‐tocopherol on β‐amyloid‐(1–42)‐induced learning and memory deficits in rats: implication of oxidative stress in β‐amyloid‐induced neurotoxicity in vivo , 1999 .

[28]  Bruce A. Yankner,et al.  Aging renders the brain vulnerable to amyloid β-protein neurotoxicity , 1998, Nature Medicine.

[29]  D. Butterfield,et al.  Vitamin E protects against Alzheimer's amyloid peptide (25–35)-induced changes in neocortical synaptosomal membrane lipid structure and composition , 1998, Brain Research.

[30]  E. Kato,et al.  Cerebral blood flow and oxygen metabolism in senile dementia of Alzheimer's type and vascular dementia with deep white matter changes , 1998, Neuroradiology.

[31]  K. Yoshimi,et al.  Co-injection of β-amyloid with ibotenic acid induces synergistic loss of rat hippocampal neurons , 1998, Neuroscience.

[32]  F. Condé,et al.  Partial Inhibition of Brain Succinate Dehydrogenase by 3‐Nitropropionic Acid Is Sufficient to Initiate Striatal Degeneration in Rat , 1998, Journal of neurochemistry.

[33]  M. Beal,et al.  Iodoacetate Produces Striatal Excitotoxic Lesions , 1997, Journal of neurochemistry.

[34]  M. Mattson,et al.  Impairment of Glucose and Glutamate Transport and Induction of Mitochondrial Oxidative Stress and Dysfunction in Synaptosomes by Amyloid β‐Peptide: Role of the Lipid Peroxidation Product 4‐Hydroxynonenal , 1997, Journal of neurochemistry.

[35]  P Woodbury,et al.  A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer's disease. The Alzheimer's Disease Cooperative Study. , 1997, The New England journal of medicine.

[36]  Joseph S. Beckman,et al.  Widespread Peroxynitrite-Mediated Damage in Alzheimer’s Disease , 1997, The Journal of Neuroscience.

[37]  R J Mark,et al.  Amyloid β-Peptide Impairs Glucose Transport in Hippocampal and Cortical Neurons: Involvement of Membrane Lipid Peroxidation , 1997, The Journal of Neuroscience.

[38]  S. DeKosky,et al.  Structural correlates of cognition in dementia: quantification and assessment of synapse change. , 1996, Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration.

[39]  S. Younkin,et al.  Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice , 1996, Science.

[40]  A. Privat,et al.  Reversion of β25–35-amyloid peptide-induced amnesia by NMDA receptor-associated glycine site agonists , 1996, Brain Research.

[41]  J. Geiger,et al.  Brain regional levels of adenosine and adenosine nucleotides in rats killed by high-energy focused microwave irradiation , 1996, Journal of Neuroscience Methods.

[42]  B. Siesjö,et al.  N-tert-butyl-alpha-phenylnitrone improves recovery of brain energy state in rats following transient focal ischemia. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[43]  B. Rosen,et al.  Involvement of Free Radicals in Excitotoxicity In Vivo , 1995, Journal of neurochemistry.

[44]  B. Yankner,et al.  Beta-amyloid neurotoxicity requires fibril formation and is inhibited by congo red. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[45]  M. Mattson.  Calcium and Neuronal Injury in Alzheimer's Disease , 1994, Annals of the New York Academy of Sciences.

[46]  B. Ames,et al.  Oxidative damage and mitochondrial decay in aging. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[47]  Patrizia Mecocci,et al.  Oxidative damage to mitochondrial DNA is increased in Alzheimer's disease , 1994, Annals of neurology.

[48]  B. Siesjö,et al.  Delayed treatment with the spin trap alpha-phenyl-N-tert-butyl nitrone (PBN) reduces infarct size following transient middle cerebral artery occlusion in rats. , 1994, Acta physiologica Scandinavica.

[49]  A. Privat,et al.  Inhibitors of free radical formation fail to attenuate direct β‐amyloid25–35 peptide‐mediated neurotoxicity in rat hippocampal cultures , 1994, Journal of neuroscience research.

[50]  L. Thal,et al.  Lack of long-term effects after β-amyloid protein injections in rat brain , 1994, Neurobiology of Aging.

[51]  H. Reichmann,et al.  Electron transport chain defects in Alzheimer's disease. , 1994, Neurology.

[52]  M. Mattson,et al.  β-Amyloid Peptide Free Radical Fragments Initiate Synaptosomal Lipoperoxidation in a Sequence-Specific Fashion: Implications to Alzheimer′s Disease , 1994 .

[53]  D. Price,et al.  Age‐Dependent Impairment of Mitochondrial Function in Primate Brain , 1993, Journal of neurochemistry.

[54]  Carl W. Cotman,et al.  Neurodegeneration induced by beta-amyloid peptides in vitro: the role of peptide assembly state , 1993, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[55]  C. Cotman,et al.  β-Amyloid neurotoxicity: A discussion of in vitro findings , 1992, Neurobiology of Aging.

[56]  R. Sapolsky,et al.  Failure of beta-amyloid protein fragment 25–35 to cause hippocampal damage in the rat , 1992, Neurobiology of Aging.

[57]  D. Stephenson,et al.  Implants containing β-amyloid protein are not neurotoxic to young and old rat brain , 1992, Neurobiology of Aging.

[58]  C. Cotman,et al.  Beta-amyloid increases neuronal susceptibility to injury by glucose deprivation. , 1991, Neuroreport.

[59]  A. Santamaría,et al.  Quinolinic acid is a potent lipid peroxidant in rat brain homogenates , 1991, Neurochemical Research.

[60]  D. Kirschner,et al.  Neurotrophic and neurotoxic effects of amyloid beta protein: reversal by tachykinin neuropeptides. , 1990, Science.

[61]  J. Phillis,et al.  Protection from cerebral ischemic injury in gerbils with the spin trap agent N-tert-butyl-α-phenylnitrone (PBN) , 1990, Neuroscience Letters.

[62]  L. Ang,et al.  Autopsy Samples of Alzheimer's Cortex Show Increased Peroxidation In Vitro , 1990, Journal of neurochemistry.

[63]  N. Sims,et al.  Altered metabolic properties of cultured skin fibroblasts in Alzheimer's disease , 1987, Annals of neurology.

[64]  R. Kauppinen,et al.  Synaptosomal bioenergetics. The role of glycolysis, pyruvate oxidation and responses to hypoglycaemia. , 1986, European journal of biochemistry.

[65]  W. Löscher,et al.  Improved Method for Isolating Synaptosomes from 11 Regions of One Rat Brain: Electron Microscopic and Biochemical Characterization and Use in the Study of Drug Effects on Nerve Terminal γ‐Aminobutyric Acid in Vivo , 1985, Journal of neurochemistry.

[66]  T. Mosmann.  Rapid colorimetric assay for cellular growth and survival: application to proliferation and cytotoxicity assays. , 1983, Journal of immunological methods.

[67]  C. Liang.  Metabolic control of circulation. Effects of iodoacetate and fluoroacetate. , 1977, The Journal of clinical investigation.

[68]  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.

[69]  Deborah Gustafson,et al.  Reduced risk of Alzheimer disease in users of antioxidant vitamin supplements: the Cache County Study. , 2004, Archives of neurology.

[70]  D. Gould,et al.  Nature and distribution of brain lesions in rats intoxicated with 3-nitropropionic acid: A type of hypoxic (energy deficient) brain damage , 2004, Acta Neuropathologica.

[71]  H. Brodaty,et al.  Tocopherol (Vitamin E) in Alzheimer’s Disease and Other Neurodegenerative Disorders , 2004, CNS drugs.

[72]  D. Gould,et al.  Correlation of morphologic brain lesions with physiologic alterations and blood-brain barrier impairment in 3-intropropionic acid toxicity in rats , 2004, Acta Neuropathologica.

[73]  A. A. Yakovlev,et al.  Effects of tumor necrosis factor‐alpha central administration on hippocampal damage in rat induced by amyloid beta‐peptide (25–35) , 2003, Journal of neuroscience research.

[74]  M. Traber,et al.  Mechanisms of vitamin E regulation: research over the past decade and focus on the future. , 2000, Antioxidants & redox signaling.

[75]  J. Hardy,et al.  Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes , 1998, Nature Medicine.

[76]  W. Meier-Ruge,et al.  The Significance of Glucose Turnover in the Brain in the Pathogenetic Mechanisms of Alzheimer's Disease , 1996, Reviews in the neurosciences.

[77]  D. Selkoe,et al.  Microinjection of synthetic amyloid beta-protein in monkey cerebral cortex fails to produce acute neurotoxicity. , 1993, The American journal of pathology.

[78]  H. Esterbauer,et al.  Determination of aldehydic lipid peroxidation products: malonaldehyde and 4-hydroxynonenal. , 1990, Methods in enzymology.

[79]  G. Paxinos,et al.  The Rat Brain in Stereotaxic Coordinates , 1983 .

[80]  G. Gobbel,et al.  Journal of Cerebral Blood Flow and Metabolism Excitotoxicity Is Required for Induction of Oxidative Stress and Apoptosis in Mouse Striatum by the Mitochondrial Toxin, 3-nitropropionic Acid , 2022 .