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mitochondrial
275 studies tagged mitochondrial, 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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Alzheimer disease (AD) is a progressive neurodegenerative disease that affects the elderly population with complex etiology.
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The research on aging and age-related diseases, especially the neurodegenerative diseases, is on the fast track.
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Alzheimer's disease (AD) is the most common cause of disability in individuals aged >65 years worldwide.
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Mitochondrial oxidative stress is a key pathologic factor in neurodegenerative diseases, including Alzheimer's disease.
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Oxidative stress is induced by an imbalanced redox states, involving either excessive generation of reactive oxygen species (ROS) or dysfunction of the antioxidant system.
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36/100
The depletion of zinc may enhance DNA damage by impairing DNA repair mechanisms.
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36/100
Mitochondria is one of the main source of oxidative stress (ROS), as it utilizes the oxygen for the energy production.
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Exposure to environmental toxins such as pesticides is implicated in increasing Alzheimer's disease risk.
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Neuroinflammation and mitochondrial dysfunction are common features of chronic neurodegenerative diseases of the central nervous system.
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A large body of evidence suggests that not only cerebral but also systemic oxidative stress (OxS) might be involved in the pathogenesis of late onset Alzheimer’s disease (LOAD) and vascular dementia (VAD), as well as of the prodromal phase of dementia, the so-called mild cognitive impairment (MCI).
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Mitochondria form a highly interconnected tubular network throughout the cell via a dynamic process, with mitochondrial segments fusing and breaking apart continuously.
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Melatonin acts as a pleiotropic agent in various age-related neurodegenerative diseases.
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The autophagic process is the only known mechanism for mitochondrial turnover and it has been speculated that dysfunction of autophagy may result in mitochondrial error and cellular stress.
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In recent years there has been enormous interest in researching oxidative stress.
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In the CNS, iron in several proteins is involved in many important processes such as oxygen transportation, oxidative phosphorylation, myelin production, and the synthesis and metabolism of neurotransmitters.
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Free radicals and other oxidants have gained importance in the field of biology due to their central role in various physiological conditions as well as their implication in a diverse range of diseases.
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40/100
Tauroursodeoxycholic acid (TUDCA) is the taurine conjugate of ursodeoxycholic acid (UDCA), a US Food and Drug Administration-approved hydrophilic bile acid for the treatment of certain cholestatic liver diseases.
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40/100
Neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), Amyotrophic lateral sclerosis (ALS) and retinal degeneration have been studied extensively and varying molecular mechanisms have been proposed for onset of such diseases.
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There has been much evidence demonstrating the involvement of oxidative stress in the pathology of neurological disorders.
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Sirtuins are nicotinamide adenine dinucleotide (NAD+)-dependent deacylases that have traditionally been linked with calorie restriction and aging in mammals.
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Whereas a modest expression of this transcriptional co-activator results in positive effects, a moderate to substantial overexpession may have deleterious consequences.
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Glycogen synthase kinase (GSK)-3β is a multifunctional protein that has been implicated in the pathological characteristics of Alzheimer's disease (AD), including the heightened levels of neurofibrillary tangles, amyloid-beta (Aβ), and neurodegeneration.
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Alzheimer's disease (AD) exhibits extensive oxidative stress throughout the body, being detected peripherally as well as associated with the vulnerable regions of the brain affected in disease.
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Ten years ago we first proposed the Alzheimer's disease (AD) mitochondrial cascade hypothesis.
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Alzheimer's disease (AD) is the most common neurodegenerative disease that causes dementia in the elderly.
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Oxidative stress and mitochondrial damage have been implicated in the pathogenesis of several neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis.
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Glutamate is one of the most prominent neurotransmitter in the body, present in over 50% of nervous tissue and plays an important role in neuronal excitation.
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Lipid peroxidation involves a cascade of reactions in which production of free radicals occurs selectively in the lipid components of cellular membranes.
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40/100
Mitochondrial dysfunctions cause numerous human disorders.
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It has recently been reported that iron oxide nanoparticles (Fe(3)O(4)-NPs, 30 nm) have the ability to translocate directly from the olfactory nerve to the brain.
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Aging is the main risk factor for Alzheimer's disease (AD); however, the aspects of the aging process that predispose the brain to the development of AD are largely unknown.
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The pineal product melatonin has remarkable antioxidant properties.
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Neurodegenerative diseases are a large group of disabling disorders of the nervous system, characterized by the relative selective death of neuronal subtypes.
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Mitochondria are involved in ATP supply to cells through oxidative phosphorylation (OXPHOS), synthesis of key molecules and response to oxidative stress, as well as in apoptosis.
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Dietary and metabolic therapies have been attempted in a wide variety of neurological diseases, including epilepsy, headache, neurotrauma, Alzheimer disease, Parkinson disease, sleep disorders, brain cancer, autism, pain, and multiple sclerosis.
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Oxidative stress and mitochondrial damage are implicated in the evolution of neurodegenerative diseases.
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Redox degenerative reactions of the biological system inevitably produce reactive oxygen species (ROS) and their derivatives.
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The importance of micronutrients in health and nutrition is undisputable, and among them, zinc is an essential element whose significance to health is increasingly appreciated and whose deficiency may play an important role in the appearance of diseases.
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Part of the inflammatory response in Alzheimer's disease (AD) is the upregulation of the inducible nitric oxide synthase (NOS2) resulting in increased NO production.
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Increasing evidence suggests that the accumulation of amyloid beta (Aβ) in synapses and synaptic mitochondria causes synaptic mitochondrial failure and synaptic degeneration in Alzheimer's disease (AD).
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Increased muscle mitochondria are largely responsible for the increased resistance to fatigue and health benefits ascribed to exercise training.
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For the past 40 years or so, oxidative stress has been increasingly recognized as a contributing factor in aging and in various forms of pathophysiology generally associated with aging.
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The pathological processes of neurodegenerative disorders such as Alzheimer's and Parkinson's diseases engender synaptic and neuronal cell damage.
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The purpose of our study was to better understand the relationship between mitochondrial structural proteins, particularly dynamin-related protein 1 (Drp1) and amyloid beta (Aβ) in the progression of Alzheimer's disease (AD).
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Detailed studies in the past two decades have shown that redox active metals like iron (Fe), copper (Cu), chromium (Cr), cobalt (Co) and other metals undergo redox cycling reactions and possess the ability to produce reactive radicals such as superoxide anion radical and nitric oxide in biological systems.
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Epigenetic modifications represent mechanisms by which cells may effectively translate multiple signaling inputs into phenotypic outputs.
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Synaptic dysfunction and the loss of synapses are early pathological features of Alzheimer's disease (AD).
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Biochemical analysis of amyloid plaques revealed that the main constituent is fibrillar aggregates of a 39-42 residue peptide referred to as the amyloid-β protein (Aβ).
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Oxidative stress (OS), caused by the imbalance between the generation and detoxification of reactive oxygen and nitrogen species (ROS/RNS), plays an important role in brain aging, neurodegenerative diseases, and other related adverse conditions, such as ischemia.
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Alzheimer disease is an age-related neurodegenerative disorder characterized by amyloid-beta (Abeta) peptide deposition into cerebral amyloid plaques.
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.
- Multifunctional roles of zinc in Alzheimer's disease
- Protein carbonyl groups as biomarkers of oxidative stress
- Alzheimer's Disease and Parkinson's Disease: A Nutritional Toxicology Perspective of the Impact of Oxidative Stress, Mitochondrial Dysfunction, Nutrigenomics and Environmental Chemicals
- Constraint Based Metabolic Modeling Identifies Robust Biomarkers and Therapeutic Target Combinations in Alzheimer Disease
- High-throughput profiling of the mitochondrial proteome using affinity fractionation and automation
- Mitochondrial DNA copy number in neurodegenerative diseases: a global meta-analysis of 156 comparisons across 76 studies
- Spermine inhibits ferroptosis in vascular dementia rats by intervening Nrf2/SLC7A11/GPX4 expression in chondriosome
- Oxidative stress-mediated neuroinflammation in Alzheimer's disease
- Increased lipid peroxidation precedes amyloid plaque formation in an animal model of Alzheimer amyloidosis