Mechanism of Oxidative Stress in Neurodegeneration

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PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin

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Oxidatively modified proteins in aging and disease1,2 1Guest Editor: Earl Stadtman 2This article is part of a series of reviews on “Oxidatively Modified Proteins in Aging and Disease.” The full list of papers may be found on the homepage of the journal.

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NADPH oxidase

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Parkinson's Disease α-Synuclein Transgenic Mice Develop Neuronal Mitochondrial Degeneration and Cell Death

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Three Distinct Mechanisms Generate Oxygen Free Radicals in Neurons and Contribute to Cell Death during Anoxia and Reoxygenation

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

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PINK1-Associated Parkinson's Disease Is Caused by Neuronal Vulnerability to Calcium-Induced Cell Death

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Glutathione Pathways in the Brain

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PINK1 Is Necessary for Long Term Survival and Mitochondrial Function in Human Dopaminergic Neurons

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The Parkinsonism-inducing Drug 1-Methyl-4-phenylpyridinium Triggers Intracellular Dopamine Oxidation

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Evidence of Oxidative Stress in Alzheimer's Disease Brain and Antioxidant Therapy

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Molecular indices of oxidative stress and mitochondrial dysfunction occur early and often progress with severity of Alzheimer's disease

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Activation of NADPH Oxidase in Alzheimer's Disease Brains

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Amyloid beta peptide and NMDA induce ROS from NADPH oxidase and AA release from cytosolic phospholipase A₂ in cortical neurons

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NADPH Oxidase-Derived Reactive Oxygen Species Mediate the Cerebrovascular Dysfunction Induced by the Amyloid β Peptide

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Neurotoxic Aβ peptides increase oxidative stress in vivo through NMDA‐receptor and nitric‐oxide‐synthase mechanisms, and inhibit complex IV activity and induce a mitochondrial permeability transition in vitro

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Uncoupling Protein-2 Is Critical for Nigral Dopamine Cell Survival in a Mouse Model of Parkinson's Disease

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Cyclophilin D in mitochondrial pathophysiology

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Oxidative damage to DNA in lymphocytes from AD patients

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The role of an astrocytic NADPH oxidase in the neurotoxicity of amyloid beta peptides

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The Origins of Oxidant Stress in Parkinson's Disease and Therapeutic Strategies

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Dysfunctions of Cellular Oxidative Metabolism in Patients with Mutations in the NDUFS1 and NDUFS4 Genes of Complex I

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CLIC1 Function Is Required for β-Amyloid-Induced Generation of Reactive Oxygen Species by Microglia

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Oxidative Stress Involvement inα-Synuclein Oligomerization in Parkinson's Disease Cybrids

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Oxidative insults induce DJ-1 upregulation and redistribution: Implications for neuroprotection

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Fibrillar β-Amyloid-stimulated Intracellular Signaling Cascades Require Vav for Induction of Respiratory Burst and Phagocytosis in Monocytes and Microglia

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Mechanism of neurodegeneration of neurons with mitochondrial DNA mutations

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Reactive Oxygen Species as Causal Agents in the Neurotoxicity of the Alzheimer's Disease‐Associated Amyloid Beta Peptidea

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Pharmacological inhibition of neuronal NADPH oxidase protects against 1-methyl-4-phenylpyridinium (MPP+)-induced oxidative stress and apoptosis in mesencephalic dopaminergic neuronal cells

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Dopamine Induces Ca2+ Signaling in Astrocytes through Reactive Oxygen Species Generated by Monoamine Oxidase

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Mitochondrial Respiratory Dysfunction in Familiar Parkinsonism Associated with PINK1 Mutation

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Antioxidants, Supplements, and Parkinson's Disease

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Targeting mitochondrial dysfunction in neurodegenerative disease: Part II

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Mitochondria and Antioxidant Targeted Therapeutic Strategies for Alzheimer's Disease

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Antimycin-insensitive oxidation of succinate and reduced nicotinamide-adenine dinucleotide in electron-transport particles II. Steroid effects

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Mechanism of neuroprotection of melatonin against beta-amyloid neurotoxicity

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Effect of beta-amyloid peptide fragment 25-35 on nonselective permeability of mitochondria.

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Effects of amyloid-beta peptides on hydrogen peroxide-metabolizing enzymes in rat brainin vivo

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Hyperoxia Produces Neuronal Necrosis in the Rat

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Motor complications, levodopa metabolism and progression of Parkinson's disease

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Amyloid-β peptide induces temporal membrane biphasic changes in astrocytes through cytosolic phospholipase A2

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Neurotoxic Mechanisms by Alzheimer's Disease-Linked N141I Mutant Presenilin 2

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Cysteinyl‐glycine reduction as marker for levodopa‐induced oxidative stress in Parkinson's disease patients

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Promethazine protects against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity

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Amino‐ and carboxyl‐terminal mutants of presenilin 1 cause neuronal cell death through distinct toxic mechanisms: Study of 27 different presenilin 1 mutants

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Allopurinol suppresses para-nonylphenol and 1-methyl-4-phenylpyridinium ion (MPP+)-induced hydroxyl radical generation in rat striatum

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Oxidative stress and dementia: new perspectives in AD pathogenesis

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New small molecules for the treatment of Parkinson's disease

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Cytotoxic mechanisms by M239V presenilin 2, a little‐analyzed Alzheimer's disease‐causative mutant

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[Morphological analysis of the reaction of the animal brain to short-term hyperoxia].

1988 • 1 citations

Deleted Work

1955 • 0 citations