ReviewMolecules (Basel, Switzerland)2009
Neuroprotection by radical avoidance: search for suitable agents.
Review in Molecules (Basel, Switzerland), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 64 citations in OpenAlex.
- Melatonin Targets Mitochondrial Redox Homeostasis: Optimizing the Intracellular Microenvironment.International journal of molecular sciences · 2026Review
- α-Phenyl-Antioxidants (Basel, Switzerland) · 2024Review
- Mechanisms and clinical evidence to support melatonin's use in severe COVID-19 patients to lower mortality.Life sciences · 2022Review
- Obstructive sleep apnea and multiple facets of a neuroinflammatory response: a narrative review.Journal of thoracic disease · 2022Review
- Neurodegeneration, memory loss, and dementia: the impact of biological clocks and circadian rhythm.Frontiers in bioscience (Landmark edition) · 2021Review
- Cognitive Impairment and Dementia: Gaining Insight through Circadian Clock Gene Pathways.Biomolecules · 2021Review
- Melatonin, Its Metabolites and Their Interference with Reactive Nitrogen Compounds.Molecules (Basel, Switzerland) · 2021Review
- Targeting Host Defense System and Rescuing Compromised Mitochondria to Increase Tolerance against Pathogens by Melatonin May Impact Outcome of Deadly Virus Infection Pertinent to COVID-19.Molecules (Basel, Switzerland) · 2020Review
- Nicotinamide: Oversight of Metabolic Dysfunction Through SIRT1, mTOR, and Clock Genes.Current neurovascular research · 2020Review
- Aging, Melatonin, and the Pro- and Anti-Inflammatory Networks.International journal of molecular sciences · 2019Review
- Toxic Synergism Between Quinolinic Acid and Glutaric Acid in Neuronal Cells Is Mediated by Oxidative Stress: Insights to a New Toxic Model.Molecular neurobiology · 2018Article
- Mitochondria: Central Organelles for Melatonin's Antioxidant and Anti-Aging Actions.Molecules (Basel, Switzerland) · 2018Review
- Melatonin and the electron transport chain.Cellular and molecular life sciences : CMLS · 2017Review
- 1,4-Dihydropyridine Derivatives: Dihydronicotinamide Analogues-Model Compounds Targeting Oxidative Stress.Oxidative medicine and cellular longevity · 2016Review
- Melatonin and Nitrones As Potential Therapeutic Agents for Stroke.Frontiers in aging neuroscience · 2016Article
- Melatonin modulates microsomal PGE synthase 1 and NF-E2-related factor-2-regulated antioxidant enzyme expression in LPS-induced murine peritoneal macrophages.British journal of pharmacology · 2014Article
- Melatonin antioxidative defense: therapeutical implications for aging and neurodegenerative processes.Neurotoxicity research · 2013Review
- Potentially neuroprotective gene modulation in an in vitro model of mild traumatic brain injury.Molecular and cellular biochemistry · 2013Article
- Melatonin in aging and disease -multiple consequences of reduced secretion, options and limits of treatment.Aging and disease · 2012Article
- Neurobiology, pathophysiology, and treatment of melatonin deficiency and dysfunction.TheScientificWorldJournal · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurodegeneration is frequently associated with damage by free radicals. However, increases in reactive oxygen and nitrogen species, which may ultimately lead to neuronal cell death, do not necessarily reflect its primary cause, but can be a consequence of otherwise induced cellular dysfunction. Detrimental processes which promote free radical formation are initiated, e.g., by disturbances in calcium homeostasis, mitochondrial malfunction, and an age-related decline in the circadian oscillator system. Free radicals generated at high rates under pathophysiological conditions are insufficiently detoxified by scavengers. Interventions at the primary causes of dysfunction, which avoid secondary rises in radical formation, may be more efficient. The aim of such approaches should be to prevent calcium overload, to reduce mitochondrial electron dissipation, to support electron transport capacity, and to avoid circadian perturbations. L-theanine and several amphiphilic nitrones are capable of counteracting excitotoxicity and/or mitochondrial radical formation. Resveratrol seems to promote mitochondrial biogenesis. Mitochondrial effects of leptin include attenuation of electron leakage. Melatonin combines all the requirements mentioned, additionally regulates anti- and pro-oxidant enzymes and is, with few exceptions, very well tolerated. In this review, the perspectives, problems and limits of drugs are compared which may be suitable for reducing the formation of free radicals.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.