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Oxidative stress in neurodegeneration: cause or consequence?
103/103 checkable references clean · checked 2026-07-23
Every reference with a DOI in the deposited reference list resolved to a known work in Crossref or DataCite at the dated check, and none carried a retraction, withdrawal, or removal notice.
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The 103 checked references that resolve
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Evidence that amyloid beta-peptide-induced lipid peroxidation and its sequelae in Alzheimer’s disease brain contribute to neuronal death1
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Basal Lipid Peroxidation in Substantia Nigra Is Increased in Parkinson's Disease
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Protein modification by the lipid peroxidation product 4‐hydroxynonenal in the spinal cords of amyotrophic lateral sclerosis patients
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Increased 3‐nitrotyrosine in both sporadic and familial amyotrophic lateral sclerosis
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Nitration of manganese superoxide dismutase in cerebrospinal fluids is a marker for peroxynitrite-mediated oxidative stress in neurodegenerative diseases
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Oxidative Damage Linked to Neurodegeneration by Selective α-Synuclein Nitration in Synucleinopathy Lesions
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Superoxide dismutase activity in Alzheimer's disease: possible mechanism for paired helical filament formation
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Decrease in Peptide Methionine Sulfoxide Reductase in Alzheimer's Disease Brain
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Alterations in the distribution of glutathione in the substantia nigra in Parkinson's disease
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Epidemiology of mutations in superoxide dismutase in amyotrophic lateal sclerosis
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Relationship of oxygen radical-induced lipid peroxidative damage to disease onset and progression in a transgenic model of familial ALS
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Oxidative damage to mitochondrial DNA in spinal motoneurons of transgenic ALS mice
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Enhanced N-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Toxicity in Mice Deficient in CuZn-Superoxide Dismutase or Glutathione Peroxidase
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Mice Deficient in Cellular Glutathione Peroxidase Show Increased Vulnerability to Malonate, 3-Nitropropionic Acid, and 1-Methyl-4-Phenyl-1,2,5,6-Tetrahydropyridine
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Transgenic mice with increased Cu/Zn-superoxide dismutase activity are resistant to N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity
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Mice with a Partial Deficiency of Manganese Superoxide Dismutase Show Increased Vulnerability to the Mitochondrial Toxins Malonate, 3-Nitropropionic Acid, and MPTP
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Manganese Superoxide Dismutase Overexpression Attenuates MPTP Toxicity
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Inhibition of neuronal nitric oxide synthase protects against MPTP toxicity
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Inducible nitric oxide synthase stimulates dopaminergic neurodegeneration in the MPTP model of Parkinson disease
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Deficiency of Inducible Nitric Oxide Synthase Protects Against MPTP Toxicity In Vivo
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Minocycline prevents nigrostriatal dopaminergic neurodegeneration in the MPTP model of Parkinson's disease
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Effects of Tocopherol and Deprenyl on the Progression of Disability in Early Parkinson's Disease
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Benefit of vitamin E, riluzole, and gababapentin in a transgenic model of familial amyotrophic lateral sclerosis
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Treatment with arimoclomol, a coinducer of heat shock proteins, delays disease progression in ALS mice
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Up‐Regulation of Protein Chaperones Preserves Viability of Cells Expressing Toxic Cu/Zn‐Superoxide Dismutase Mutants Associated with Amyotrophic Lateral Sclerosis
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Hsp70 and Hsp40 improve neurite outgrowth and suppress intracytoplasmic aggregate formation in cultured neuronal cells expressing mutant SOD1
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α-Synuclein Overexpression Protects against Paraquat-Induced Neurodegeneration
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Kinetic Stabilization of the α-Synuclein Protofibril by a Dopamine-α-Synuclein Adduct
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Vesicle Permeabilization by Protofibrillar α-Synuclein Is Sensitive to Parkinson's Disease-Linked Mutations and Occurs by a Pore-like Mechanism
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Impaired dopamine storage resulting from alpha-synuclein mutations may contribute to the pathogenesis of Parkinson's disease
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Dopamine-dependent neurotoxicity of α-synuclein: A mechanism for selective neurodegeneration in Parkinson disease
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Mice Lacking α-Synuclein Display Functional Deficits in the Nigrostriatal Dopamine System
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Glutathione decreases in dopaminergic PC12 cells interfere
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4-Hydroxy-2-nonenal-mediated Impairment of Intracellular Proteolysis during Oxidative Stress
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Monomeric Cu,Zn-superoxide Dismutase Is a Common Misfolding Intermediate in the Oxidation Models of Sporadic and Familial Amyotrophic Lateral Sclerosis
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α-Synuclein Promotes Mitochondrial Deficit and Oxidative Stress
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Effect of Wild-type or Mutant Parkin on Oxidative Damage, Nitric Oxide, Antioxidant Defenses, and the Proteasome
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Effect of overexpression of wild‐type and mutant Cu/Zn‐superoxide dismutases on oxidative damage and antioxidant defences: relevance to Down's syndrome and familial amyotrophic lateral sclerosis
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Effect of overexpression of wild‐type and mutant Cu/Zn‐superoxide dismutases on oxidative stress and cell death induced by hydrogen peroxide, 4‐hydroxynonenal or serum deprivation: potentiation of injury by ALS‐related mutant superoxide dismutases and protection by Bcl‐2
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ALS-Linked Cu/Zn–SOD Mutation Increases Vulnerability of Motor Neurons to Excitotoxicity by a Mechanism Involving Increased Oxidative Stress and Perturbed Calcium Homeostasis
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Peroxynitrite Mediates Neurotoxicity of Amyloid β-Peptide<sub>1–42</sub>- and Lipopolysaccharide-Activated Microglia
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Altered Glial Function Causes Neuronal Death and Increases Neuronal Susceptibility to 1‐Methyl‐4‐Phenylpyridinium‐ and 6‐Hydroxydopamine‐Induced Toxicity in Astrocytic/Ventral Mesencephalic Co‐Cultures
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Inflammatory Regulators in Parkinson's Disease: iNOS, Lipocortin-1, and Cyclooxygenases-1 and -2
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Persistent activation of p38 mitogen-activated protein kinase in a mouse model of familial amyotrophic lateral sclerosis correlates with disease progression
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Cyclooxygenase 2 inhibition protects motor neurons and prolongs survival in a transgenic mouse model of ALS
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Differential expression of inflammation‐ and apoptosis‐related genes in spinal cords of a mutant SOD1 transgenic mouse
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Neurotoxic Mechanisms Caused by the Alzheimer's Disease-linked Swedish Amyloid Precursor Protein Mutation
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Motoneuron Death Triggered by a Specific Pathway Downstream of Fas
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MPTP Activates c‐Jun NH<sub>2</sub>‐Terminal Kinase (JNK) and Its Upstream Regulatory Kinase MKK4 in Nigrostriatal Neurons In Vivo
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SP600125, a new JNK inhibitor, protects dopaminergic neurons in the MPTP model of Parkinson’s disease
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Gene transfer of the JNK interacting protein-1 protects dopaminergic neurons in the MPTP model of Parkinson's disease
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Dopamine Neurons from Transgenic Mice with a Knockout of the p53 Gene Resist MPTP Neurotoxicity
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Apoptosis-inducing neurotoxicity of dopamine and its metabolites via reactive quinone generation in neuroblastoma cells
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Glutathione depletion switches nitric oxide neurotrophic effects to cell death in midbrain cultures: implications for Parkinson's disease
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Dopamine toxicity in neuroblastoma cells: role of glutathione depletion by l-BSO and apoptosis
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Pharmacological inactivation of the vesicular monoamine transporter can enhance 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurodegeneration of midbrain dopaminergic neurons, but not locus coeruleus noradrenergic neurons
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Increased MPTP Neurotoxicity in Vesicular Monoamine Transporter 2 Heterozygote Knockout Mice
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Murine vesicular monoamine transporter 2: molecular cloning and genomic structure
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Conjugates of Catecholamines with Cysteine and GSH in Parkinson's Disease: Possible Mechanisms of Formation Involving Reactive Oxygen Species
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Dopamine Oxidation Alters Mitochondrial Respiration and Induces Permeability Transition in Brain Mitochondria
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Indices of oxidative stress and mitochondrial function in individuals with incidental Lewy body disease
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Glutathione Depletion in PC12 Results in Selective Inhibition of Mitochondrial Complex I Activity
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Depletion of brain glutathione results in a decrease of glutathione reductase activity; an enzyme susceptible to oxidative damage
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Mutated Human SOD1 Causes Dysfunction of Oxidative Phosphorylation in Mitochondria of Transgenic Mice
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Mitochondrial dysfunction due to mutant copper/zinc superoxide dismutase associated with amyotrophic lateral sclerosis is reversed by N-acetylcysteine
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Alzheimer's disease cybrids replicate ?-amyloid abnormalities through cell death pathways
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Brain iron in the ferrocene-loaded rat: Its chelation and influence on dopamine metabolism
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Iron Acquisition and Expression of Iron Regulatory Proteins in the Developing Brain: Manipulation by Ethanol Exposure, Iron Deprivation and Cellular Dysfunction
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Genetic or Pharmacological Iron Chelation Prevents MPTP-Induced Neurotoxicity In Vivo
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Treatment with a Copper-Zinc Chelator Markedly and Rapidly Inhibits β-Amyloid Accumulation in Alzheimer's Disease Transgenic Mice
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Metal-Protein Attenuation With Iodochlorhydroxyquin (Clioquinol) Targeting Aβ Amyloid Deposition and Toxicity in Alzheimer Disease
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The Copper Chelator d‐Penicillamine Delays Onset of Disease and Extends Survival in a Transgenic Mouse Model of Familial Amyotrophic Lateral Sclerosis
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Altered Reactivity of Superoxide Dismutase in Familial Amyotrophic Lateral Sclerosis
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A gain-of-function of an amyotrophic lateral sclerosis-associated Cu,Zn-superoxide dismutase mutant: An enhancement of free radical formation due to a decrease in Km for hydrogen peroxide.
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Survival in transgenic ALS mice does not vary with CNS glutathione peroxidase activity
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Increased mitochondrial antioxidative activity or decreased oxygen free radical propagation prevent mutant SOD1‐mediated motor neuron cell death and increase amyotrophic lateral sclerosis‐like transgenic mouse survival
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Mutations in copper-zinc superoxide dismutase that cause amyotrophic lateral sclerosis alter the zinc binding site and the redox behavior of the protein.
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Induction of Nitric Oxide -- Dependent Apoptosis in Motor Neurons by Zinc-Deficient Superoxide Dismutase
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Mutant SOD1 causes motor neuron disease independent of copper chaperone–mediated copper loading
The 5 references without a DOI — listed, not checked
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no DOI — not checkedSaporito, M.S., Brown, E.M., Miller, M.S. & Carswell, S. CEP-1347/KT-7515, an inhibitor of c-Jun N-terminal kinase activation, attenuates the 1-methyl-4-phenyl tetrahydropyridine-mediated loss of nigrostriatal dopaminergic neurons in vivo. J. Pharmacol. Exp. Ther. 288, 421–427 (1999).
no DOI — not checkedStaal, R.G. & Sonsalla, P.K. Inhibition of brain vesicular monoamine transporter (VMAT2) enhances 1-methyl-4-phenylpyridinium neurotoxicity in vivo in rat striata. J. Pharmacol. Exp. Ther. 293, 336–342 (2000).
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