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Anxiety symptoms were assessed using the Beck Anxiety Inventory, while fatigue was evaluated using the Modified Fatigue Impact Scale and the Fatigue Severity Scale. Peripheral blood samples were collected before the initiation of multiple sclerosis\u2010specific therapy. Cytokines, neurotrophic factors, neuronal\/glial injury markers, vitamin D, oxidative damage parameters, mitochondrial reactive oxygen species, mitochondrial DNA damage, inflammasome\u2010related proteins, apoptotic markers, and mitochondrial homeostasis\u2010related genes were analyzed in serum using ELISA, biochemical assays, Western blotting, and RT\u2010PCR.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Compared with healthy controls, patients with RRMS showed higher anxiety and fatigue scores, increased circulating IL\u20101\u03b2, IL\u201018, and TNF\u2010\u03b1 levels, and increased NLRP3 inflammasome expression. These alterations were accompanied by increased oxidative damage, higher mitochondrial reactive oxygen species production, increased mitochondrial 8\u2010oxoG levels, increased Bax expression, reduced Bcl\u20102 expression, decreased TFAM expression, and increased Pink\u20101 and Parkin expression. In addition, patients exhibited increased serum levels of S100\u03b2 and neuron\u2010specific enolase, along with reduced brain\u2010derived neurotrophic factor (BDNF) and nerve growth factor (NGF) levels. Exploratory correlation analyses suggested biologically plausible associations among neurotrophic signaling, mitochondrial biogenesis, inflammatory activation, oxidative stress, and markers of neuronal\/glial injury.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These findings suggest that treatment\u2010na\u00efve RRMS is characterized by a peripheral inflammatory\u2013mitochondrial imbalance associated with fatigue, anxiety, increased neuronal\/glial injury markers, and reduced neurotrophic support. Peripheral biomarkers such as S100\u03b2, neuron\u2010specific enolase, BDNF, and mitochondrial homeostasis\u2010related markers may represent accessible candidate indicators of disease\u2010related biological alterations.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/brb3.71707","type":"journal-article","created":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T04:43:26Z","timestamp":1787719406000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Associations Between Neuromuscular Fatigue, Anxiety, and Peripheral Biomarkers of Neuronal Injury, Inflammation, and Mitochondrial Dysfunction in Treatment\u2010Na\u00efve Relapsing\u2010Remitting Multiple Sclerosis"],"prefix":"10.1002","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1835-4152","authenticated-orcid":false,"given":"Amanda V.","family":"Steckert","sequence":"first","affiliation":[{"name":"Graduate Program in Health Management 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