Resting-state neural oscillations of the motor system influence the resting motor threshold.

Multiple sclerosis (MS) is one of the most complex and disabling neurological diseases of our time, with an unpredictable course and multiple symptoms that can affect millions around the world (–). This chronic autoimmune disease manifests through the immune system’s misguided attack on the central nervous system, leading to inflammation, demyelination, and subsequent neurological dysfunction (). As medical science continues to grapple with the challenges of MS management, researchers have increasingly turned their attention to natural compounds that might offer novel therapeutic avenues. Among these, flavonoids, a diverse group of plant-derived polyphenolic compounds have emerged as particularly promising candidates for MS intervention (–). This structured narrative review summarizes current evidence on flavonoids in MS relevant experimental and human studies, with attention to mechanisms, translational barriers and future research needs. This review was prepared as a structured narrative review rather than a formal systematic review or meta-analysis. Literature searches were conducted from database inception to December 2025. Relevant literature was identified using PubMed, MEDLINE, Scopus, Web of Science, Google Scholar and ClinicalTrials.gov. Searches combined terms for multiple sclerosis and related models, including “multiple sclerosis”, “experimental autoimmune encephalomyelitis”, “EAE”, “cuprizone”, “demyelination” and “remyelination”, with terms for flavonoids and named compounds, including “flavonoid”, “flavonol”, “flavone”, “flavanone”, “isoflavone”, “anthocyanidin”, “flavanol”, “quercetin”, “EGCG”, “hesperidin”, “luteolin”, “rutin”, “baicalein”, “apigenin’, “kaempferol”, “genistein” and “naringenin”. Additional searches covered neuroinflammation, “NFκB”, “Nrf2”, “TLR MyD88”, “inflammasome”, “microglia”, “oligodendrocyte precursor cells”, “blood brain barrier”, “pharmacokinetics”, “metabolism”, “safety”, and “disease modifying therapy interactions”. We prioritized MS specific human studies, randomized controlled trials, EAE studies, cuprizone demyelination studies and relevant CNS, immune cell or blood brain barrier models. Studies from other neurological disease models or non-neurological systems were used only when they clarified mechanisms that could be relevant to MS, and these were described as indirect evidence. Because this article was designed as a structured narrative review, searches were iterative and topic driven rather than PRISMA based. Therefore, formal duplicate independent screening, a PRISMA flow diagram, and exact numerical screening counts were not generated. To improve transparency, studies were selected when they provided direct or mechanistic evidence relevant to flavonoids, flavonoid related compounds, MS, EAE, cuprizone demyelination, remyelination, neuroinflammation, oxidative stress, glial activation, blood brain barrier transport, pharmacokinetics, metabolism, safety, or interactions with disease modifying therapies. Inclusion criteria were English language primary research or high-quality review articles reporting flavonoid or flavonoid related effects on MS, demyelination, neuroinflammation, oxidative stress, glial activation, remyelination, pharmacokinetics, metabolism, safety or blood brain barrier transport.