Oxidative Stress Signaling in Alzheimers Disease

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Mitochondrial abnormalities in Alzheimer's disease

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Iron accumulation in Alzheimer disease is a source of redox-generated free radicals

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ABAD Directly Links Aß to Mitochondrial Toxicity in Alzheimer's Disease

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Widespread Peroxynitrite-Mediated Damage in Alzheimer’s Disease

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Evidence of oxidative damage in Alzheimer's disease brain: central role for amyloid β-peptide

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The Aβ Peptide of Alzheimer's Disease Directly Produces Hydrogen Peroxide through Metal Ion Reduction

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Mitochondria are a direct site of Aβ accumulation in Alzheimer's disease neurons: implications for free radical generation and oxidative damage in disease progression

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4‐Hydroxynonenal‐Derived Advanced Lipid Peroxidation End Products Are Increased in Alzheimer's Disease

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Amyloid beta, mitochondrial dysfunction and synaptic damage: Implications for cognitive decline in aging and Alzheimer’s disease

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Oxidative damage in Alzheimer's

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Accumulation of amyloid precursor protein in the mitochondrial import channels of human Alzheimer's disease brain is associated with mitochondrial dysfunction

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A Role for 4‐Hydroxynonenal, an Aldehydic Product of Lipid Peroxidation, in Disruption of Ion Homeostasis and Neuronal Death Induced by Amyloid β‐Peptide

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Increased Lipid Peroxidation Precedes Amyloid Plaque Formation in an Animal Model of Alzheimer Amyloidosis

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RNA Oxidation Is a Prominent Feature of Vulnerable Neurons in Alzheimer’s Disease

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Review: Alzheimer's Amyloid β-Peptide-Associated Free Radical Oxidative Stress and Neurotoxicity

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Advanced Maillard reaction end products are associated with Alzheimer disease pathology.

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Four-hydroxynonenal, a product of lipid peroxidation, is increased in the brain in Alzheimer's disease

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Elevated thiobarbituric acid-reactive substances and antioxidant enzyme activity in the brain in Alzheimer's disease

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Evidence of neuronal oxidative damage in Alzheimer's disease.

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Energetic basis of brain activity: implications for neuroimaging

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Metalloenzyme-like Activity of Alzheimer's Disease β-Amyloid

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Glycated tau protein in Alzheimer disease: a mechanism for induction of oxidant stress.

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Alzheimer's brains harbor somatic mtDNA control-region mutations that suppress mitochondrial transcription and replication

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Amyloid β-Peptide Impairs Glucose Transport in Hippocampal and Cortical Neurons: Involvement of Membrane Lipid Peroxidation

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Proteomic identification of nitrated proteins in Alzheimer's disease brain

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Cell-cycle reentry and cell death in transgenic mice expressing nonmutant human tau isoforms

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Electron transport chain defects in Alzheimer's disease brain

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Myeloperoxidase-generated reactive nitrogen species convert LDL into an atherogenic form in vitro

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β-Amyloid Induces Neuronal Apoptosis Via a Mechanism that Involves the c-Jun N-Terminal Kinase Pathway and the Induction of Fas Ligand

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A selective defect of cytochrome c oxidase is present in brain of Alzheimer disease patients

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Radical AGEing in Alzheimer's disease

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Activation and redistribution of c‐Jun N‐terminal kinase/stress activated protein kinase in degenerating neurons in Alzheimer's disease

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Heme oxygenase-1 is associated with the neurofibrillary pathology of Alzheimer's disease.

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The toxicity in vitro of β-amyloid protein

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Non-enzymatically glycated tau in Alzheimer's disease induces neuronal oxidant stress resulting in cytokine gene expression and release of amyloid β-peptide

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Activation of p38 Kinase Links Tau Phosphorylation, Oxidative Stress, and Cell Cycle-Related Events in Alzheimer Disease

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Redox-active iron mediates amyloid-β toxicity

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p38 Kinase Is Activated in the Alzheimer's Disease Brain

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Role of mitochondrial dysfunction in Alzheimer's disease

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Phosphorylation Sites on Tau Identified by Nanoelectrospray Mass Spectrometry

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Immunohistochemical evidence of oxidative [corrected] stress in Alzheimer's disease.

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The myeloperoxidase system of human phagocytes generates Nε-(carboxymethyl)lysine on proteins: a mechanism for producing advanced glycation end products at sites of inflammation

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Abnormalities of mitochondrial enzymes in Alzheimer disease

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Carboxyl-terminal-truncated apolipoprotein E4 causes Alzheimer's disease-like neurodegeneration and behavioral deficits in transgenic mice

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Oxidative stress activates a positive feedback between the γ‐ and β‐secretase cleavages of the β‐amyloid precursor protein

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Gene expression profiles of transcripts in amyloid precursor protein transgenic mice: up-regulation of mitochondrial metabolism and apoptotic genes is an early cellular change in Alzheimer's disease

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β‐Site APP cleaving enzyme up‐regulation induced by 4‐hydroxynonenal is mediated by stress‐activated protein kinases pathways

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Neuronal Oxidative Stress Precedes Amyloid-β Deposition in Down Syndrome

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Myeloperoxidase Polymorphism Is Associated with Gender Specific Risk for Alzheimer's Disease

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Lipid- and receptor-binding regions of apolipoprotein E4 fragments act in concert to cause mitochondrial dysfunction and neurotoxicity

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Differential activation of neuronal ERK, JNK/SAPK and p38 in Alzheimer disease: the ‘two hit’ hypothesis

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Phosphorylation of microtubule‐associated protein tau by stress‐activated protein kinases

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Alzheimer's disease – synergistic effects of glucose deficit, oxidative stress and advanced glycation endproducts

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Abnormal Mitochondrial Morphology in Sporadic Parkinson's and Alzheimer's Disease Cybrid Cell Lines

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Activation of c-Jun N-Terminal Kinase and p38 in an Alzheimer's Disease Model Is Associated with Amyloid Deposition

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Ribosomal RNA in Alzheimer Disease Is Oxidized by Bound Redox-active Iron

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Advanced glycation endproducts in ageing and Alzheimer's disease

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Calcium homeostasis and reactive oxygen species production in cells transformed by mitochondria from individuals with sporadic Alzheimer's disease

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Carbonyl‐Related Posttranslational Modification of Neurofilament Protein in the Neurofibrillary Pathology of Alzheimer's Disease

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Tau phosphorylation in Alzheimer's disease: pathogen or protector?

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Increased regional brain concentrations of ceruloplasmin in neurodegenerative disorders

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Decrease and Structural Modifications of Phosphatidylethanolamine Plasmalogen in the Brain with Alzheimer Disease

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Aberrant expression of NOS isoforms in Alzheimer's disease is structurally related to nitrotyrosine formation.

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Amyloid-β Peptides Are Cytotoxic to Oligodendrocytes

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Phosphorylation of tau antagonizes apoptosis by stabilizing β-catenin, a mechanism involved in Alzheimer's neurodegeneration

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Correlation of Astrocytic S100β Expression with Dystrophic Neurites in Amyloid Plaques of Alzheimerʼs Disease

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beta-Amyloid-induced neuronal apoptosis requires c-Jun N-terminal kinase activation

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Cytochemical Demonstration of Oxidative Damage in Alzheimer Disease by Immunochemical Enhancement of the Carbonyl Reaction with 2,4-Dinitrophenylhydrazine

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Impairment in mitochondrial cytochrome oxidase gene expression in Alzheimer disease.

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Oxidative stress potentiates BACE1 gene expression and A? generation

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