ReviewNutrients2019
A Review of Various Antioxidant Compounds and their Potential Utility as Complementary Therapy in Multiple Sclerosis.
Review in Nutrients, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 3 of them syntheses that pooled it.
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
52 citing papers in PubMed, 3 syntheses or guidelines pooled it, 101 citations in OpenAlex.
- Association of Polyunsaturated Fatty Acid Intake on Inflammatory Gene Expression and Multiple Sclerosis: A Systematic Review and Meta-Analysis.Nutrients · 2022Pooled it
- Efficacy of diet on fatigue, quality of life and disability status in multiple sclerosis patients: rapid review and meta-analysis of randomized controlled trials.BMC neurology · 2022Pooled it
- Role of lipoic acid in multiple sclerosis.CNS neuroscience & therapeutics · 2022Pooled it
- Paeonol as a Multi-Target Therapy for Neurological Disorders: Mechanistic Insights Into Neuroprotection.Immunity, inflammation and disease · 2026Review
- The Diet-Multiple Sclerosis Connection: Oxidative Stress and Emerging Mechanisms.Molecular neurobiology · 2026Review
- Is Obesity a Modifiable Risk Factor in Multiple Sclerosis? Mechanistic Insights into Neuroinflammation and Oxidative Damage.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Dysbiosis and Therapeutic Modulation of the Gut Microbiota in Multiple Sclerosis: A Narrative Review.Health science reports · 2025Article
- An assessment of an antioxidative status in patients with multiple sclerosis using standard biochemical analyses.Journal of medical biochemistry · 2025Article
- Article
- Repair mechanisms of the central nervous system: From axon sprouting to remyelination.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Lycopene Supplemented Mediterranean Diet Ameliorates Experimental Autoimmune Encephalomyelitis (EAE) in Mice and Changes Intestinal Microbiome.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Anti-inflammatory potential of royal jelly in multiple sclerosis disease: a double randomized clinical trial.Annals of medicine and surgery (2012) · 2025Article
- Emerging Insights into the Role of Macrophages in Multiple Sclerosis: Pathogenesis and Potential Therapeutic Strategies.Journal of inflammation research · 2025Review
- Oxidative/Nitrosative Stress, Apoptosis, and Redox Signaling: Key Players in Neurodegenerative Diseases.Journal of biochemical and molecular toxicology · 2025Review
- Exploration of the Role of Vitamins in Preventing Neurodegenerative Diseases: Comprehensive Review on Preclinical and Clinical Findings.Current neuropharmacology · 2025Review
- Sevoflurane Alters Serum Metabolites in Elders and Aging Mice and Increases Inflammation in Hippocampus.Journal of inflammation research · 2024Article
- Beneficial Effects of Plant Oils Supplementation on Multiple Sclerosis: A Comprehensive Review of Clinical and Experimental Studies.Nutrients · 2023Review
- Unlocking Potentially Therapeutic Phytochemicals in Capadulla (Metabolites · 2023Article
- Treatment with the Olive Secoiridoid Oleacein Protects against the Intestinal Alterations Associated with EAE.International journal of molecular sciences · 2023Article
- Fasting: From Physiology to Pathology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Multiple sclerosis (MS) is a complex disease of the central nervous system (CNS). The etiology of this multifactorial disease has not been clearly defined. Conventional medical treatment of MS has progressed, but is still based on symptomatic treatment. One of the key factors in the pathogenesis of MS is oxidative stress, enhancing inflammation and neurodegeneration. In MS, both reactive oxygen and nitrogen species are formed in the CNS mainly by activated macrophages and microglia structures, which can lead to demyelination and axon disruption. The course of MS is associated with the secretion of many inflammatory and oxidative stress mediators, including cytokines (IL-1b, IL-6, IL-17, TNF-α, INF-γ) and chemokines (MIP-1a, MCP-1, IP10). The early stage of MS (RRMS) lasts about 10 years, and is dominated by inflammatory processes, whereas the chronic stage is associated with neurodegenerative axon and neuron loss. Since oxidative damage has been known to be involved in inflammatory and autoimmune-mediated processes, antioxidant therapy could contribute to the reduction or even prevention of the progression of MS. Further research is needed in order to establish new aims for novel treatment and provide possible benefits to MS patients. The present review examines the roles of oxidative stress and non-pharmacological anti-oxidative therapies in MS.
Indexed as
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What Socratic 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 Socratic graph.