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oxidative
275 studies tagged oxidative, dated 1989-01-01 to 2026-10-23. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Pantethine and Neurodegeneration: A Coenzyme A-Centered Framework Linking Metabolism, Neuroinflammation, and Mitochondrial Dysfunction 2026-10-23
- BNIP3L/NIX-mediated mitophagy limits Alzheimer’s disease pathology and preserves neuronal function 2026-10-20
- Convergent Mitochondrial and Oxidative Stress Signatures in Spaceflight and Tauopathy: A Comparative Multi-Omics Reanalysis in Drosophila melanogaster 2026-10-19
Studies
275 studies carry this tag.
Date range
1989 to 2026
Top journals
- The Journal of neuroscience : the official journal of the Society for Neuroscience 9
- Free radical biology & medicine 8
- Redox biology 8
- Proceedings of the National Academy of Sciences of the United States of America 7
- Biochimica et biophysica acta 6
168 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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Neurodegenerative diseases are a growing global health burden associated with aging and characterized by progressive neuronal dysfunction, metabolic failure, mitochondrial impairment, oxidative stress, and chronic neuroinflammation.
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16/100
Defective mitophagy is emerging as a key contributor to Alzheimer’s disease (AD), but the neuronal pathways governing mitochondrial clearance and their contribution to disease progression remain poorly understood.
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Mitochondrial dysfunction is a shared biological thread between terrestrial Alzheimer’s disease (AD) and in the unique stress environment of spaceflight, making mitochondrial pathophysiology a compelling target for comparative investigation.
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Alzheimer’s disease (AD) involves widespread metabolic, mitochondrial, inflammatory, and redox dysfunction.
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Alzheimer’s disease involves progressive necroptosis of neurons, and the associated cognitive deficits can be mitigated by inhibiting cAMP-degrading phosphodiesterase 4D (PDE4D).
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These data further support the use of the LOAD2.Mthfr 677C>T mouse model to study aspects of ADRD such as cerebrovascular compromise.
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Spermine exerts neuroprotective effects in VaD by inhibiting TRPM2-mediated oxidative stress and activating the Nrf2/SLC7A11/GPX4 pathway, thereby suppressing ferroptosis.
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Although endoplasmic reticulum (ER) stress and maladaptive unfolded protein response (UPR) are increasingly implicated in Alzheimer’s disease (AD), the influence of vitamin D (VitD) on these mechanisms remains unclear.
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Traumatic brain injury (TBI) is a risk factor for Alzheimer’s disease (AD), and both conditions are associated with impaired glucose metabolism and mitochondrial dysfunction.
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Apigenin is an abundant, bioactive phytochemical with reported therapeutic potential and neuroprotective effects in a variety of age-related disease models.
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Consequently, changes in mitochondrial DNA copy number (mtDNA-CN), the number of mtDNA genomes per cell or tissue sample, are associated with diseases ranging from cancer and obesity to psoriasis and all-cause mortality.
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These findings identify an age-dependent breakdown of the metabolic resilience network formed by NAMPT, NAD⁺, SIRT1, and AMPK as a key mechanistic driver of metabolic stress-induced early AD-like pathology.
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Alzheimer’s disease (AD) is characterised by progressive accumulation of misfolded proteins and failure of cellular clearance pathways, particularly the autophagy–lysosomal system.
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Transactive response DNA-binding protein 43 (TDP-43) aggregation and loss of function are hallmark features of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) among other neurodegenerative diseases.
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Cardiovascular disease and cognitive loss have a neurocardiac basis.
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Cellular senescence, once considered a protective mechanism against oncogenesis, is now recognized as a key driver of aging and age-related diseases, including Alzheimer's disease (AD).
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The AMPK/SIRT1/PGC-1α pathway represents a cornerstone target at the intersection of metabolism, aging, and disease.
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As expected, males had higher lean mass and VO2peak than females (p = 0.01), but groups did not differ in body mass index (p = 0.51).
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While mitochondria provide critical energy resources, mitochondrial dysfunction can lead to both metabolic and neurodegenerative disorders.
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Microglia play a significant role in the development and progression of Alzheimer's disease (AD).
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SUMOylation, a reversible post-translational modification, regulates various mitochondrial processes, including biogenesis, dynamics, mitophagy, and the mitochondrial unfolded protein response.
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Traumatic brain injury (TBI) is a major risk factor for neurodegenerative diseases, including Alzheimer's disease (AD), yet the mechanistic link remains unclear.
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43/100
Autophagy plays a pivotal role in the pathogenesis and progression of Alzheimer's disease (AD).
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Alzheimer's disease (AD) is the most common neurodegenerative disease, characterized by memory loss, speech and motor defects, personality changes, and psychological disorders.
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Reactive oxygen species (ROS) are metabolic by-products that constitute an indispensable component of physiological processes, albeit their heightened presence may proffer substantial perils to biological entities.
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Chronic neuroinflammation serves a key role in the onset and progression of neurodegenerative disorders.
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Considering these results, combination of mitochondria-targeted compounds with other anti-amyloid beta or anti-tau therapies hold promise as neuroprotective drugs for the prevention and/or treatment of AD.
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Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are devastating neurodegenerative diseases with no effective cure.
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41/100
Alzheimer's disease's pathophysiology is still a conundrum.
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Amyloid beta (Aβ) deposition within the brain vasculature is an early hallmark of Alzheimer's disease (AD), which triggers loss of brain vascular smooth muscle cells (BVSMCs) in cerebral arteries, via poorly understood mechanisms, altering cerebral blood flow, brain waste clearance, and promoting cognitive impairment.
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43/100
Increased levels of ROS/RNS, generated from both endogenous (mitochondria, NADPH oxidases) and/or exogenous sources (radiation, certain drugs, foods, cigarette smoking, pollution) result in a harmful condition termed oxidative stress ("bad stress").
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Mitochondria play a key role in both health and disease.
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Aging is a major risk factor for many age-associated disorders, including neurodegenerative diseases.
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The disturbance in mitochondrial functions and homeostasis are the major features of neuron degenerative conditions, like Parkinson's disease, Amyotrophic Lateral Sclerosis, and Alzheimer's disease, along with protein misfolding.
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Ferroptosis is a type of regulated cell death characterized by intracellular accumulation of iron and reactive oxygen species, inhibition of system Xc-, glutathione depletion, nicotinamide adenine dinucleotide phosphate oxidation and lipid peroxidation.
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Neurodegenerative diseases, featured by progressive loss of structure or function of neurons, are considered incurable at present.
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Oxidative stress, a state of disrupted redox signaling, reactive oxygen species (ROS) overproduction, and oxidative cell damage, accompanies numerous brain pathologies, including aging-related dementia and Alzheimer's disease, the most common neurodegenerative disorder of the elderly population.
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In total, twenty elements appear to be essential for the correct functioning of the human body, half of which are metals and half are non-metals.
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Oxidative stress has been linked with a variety of diseases, being involved in the debut and/or progress of several neurodegenerative disorders.
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41/100
Alzheimer's disease (AD) is one of the major worldwide causes of dementia that is characterized by irreversible decline in learning, memory loss, and behavioral impairments.
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As the number of patients with Alzheimer's disease (AD) increases, it brings great suffering to their families and causes a heavy socioeconomic burden to society.
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Oxidative stress plays an important role in the development of aging-related diseases by accelerating the lipid peroxidation of polyunsaturated fatty acids in the cell membrane, resulting in the production of aldehydes, such as malondialdehyde and 4-hydroxy-2-nonenal (4-HNE) and other toxic substances.
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Regarding the epidemiological studies, neurological dysfunctions caused by cerebral ischemia or neurodegenerative diseases (NDDs) have been considered a pointed matter.
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Astrocytes play key roles in the regulation of brain energy metabolism, which has a major impact on brain functions, including memory, neuroprotection, resistance to oxidative stress and homeostatic tone.
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The clearance of damaged or unwanted mitochondria by autophagy (also known as mitophagy) is a mitochondrial quality control mechanism postulated to play an essential role in cellular homeostasis, metabolism, and development and confers protection against a wide range of diseases.
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Alzheimer's disease (AD) is the most conspicuous chronic neurodegenerative syndrome, which has become a significant challenge for the global healthcare system.
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Alzheimer's disease (AD) is a progressive and fatal neurodegenerative disorder.
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Environmental exposure to neurotoxic metals and metalloids such as arsenic, cadmium, lead, mercury, or manganese is a global health concern affecting millions of people worldwide.
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Reactive oxygen species (ROS) are metabolic byproducts that are necessary for physiological function but can be toxic at high levels.
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Oxidative stress is a component of many diseases, including atherosclerosis, chronic obstructive pulmonary disease, Alzheimer disease and cancer.
From across this tag
9 of the 275 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 9. The same 9 appear here every time.
- Protein carbonyl groups as biomarkers of oxidative stress
- Ageing as a risk factor for neurodegenerative disease
- Mitochondrial unfolded protein response: An emerging pathway in human diseases
- Involvement of oxidative stress-induced abnormalities in ceramide and cholesterol metabolism in brain aging and Alzheimer's disease
- Evidence that 4-hydroxynonenal mediates oxidative stress-induced neuronal apoptosis
- Amyloid beta peptide and NMDA induce ROS from NADPH oxidase and AA release from cytosolic phospholipase A2 in cortical neurons
- Excitotoxicity: bridge to various triggers in neurodegenerative disorders
- Mitochondrial bioenergetic deficit precedes Alzheimer's pathology in female mouse model of Alzheimer's disease
- The reduction of NADH ubiquinone oxidoreductase 24- and 75-kDa subunits in brains of patients with Down syndrome and Alzheimer's disease