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We recently demonstrated soluble iron accumulation in activated microglia of sporadic ALS spinal cords. This finding could indicate that iron\u2010mediated Fenton reaction is most likely to be responsible for oxidative stress associated with this disease. The excitatory amino acid neurotoxicity hypothesis for sporadic ALS has been proposed based on increased glutamate and aspartate concentrations in cerebrospinal fluid from the patients. Initially, the increase in extracellular excitatory amino acid levels was considered to reflect excessive release from the axon terminal of upper motor neurons. However, it is a question of whether the damaged upper motor neurons continue releasing glutamate even in advanced stage of this disease. To address this issue, we hypothesized that glial cells might be a glutamate release source. Our immunohistochemical analysis on autopsied human spinal cords revealed that ferritin, hepcidin, ferroportin, aconitase 1, tumor necrosis factor\u2010\u03b1 (TNF\u2010\u03b1), TNF\u2010\u03b1\u2010converting enzyme (TACE), and glutaminase\u2010C (GAC) were expressed mainly in microglia and that cystine\/glutamate antiporter (xCT) was expressed mainly in astrocytes. We next performed cell culture experiments. Cultured microglia treated with soluble iron over\u2010released glutamate and TNF\u2010\u03b1 via aconitase 1 and TACE, respectively. Cultured microglia treated with TNF\u2010\u03b1 over\u2010released glutamate via GAC. Cultured microglia treated with hepcidin, of which expression is known to be upregulated by TNF\u2010\u03b1, showed downregulated expression of ferroportin. Cultured astrocytes treated with hydrogen peroxide over\u2010released glutamate via xCT. These observations provide <jats:italic>in vivo<\/jats:italic> and <jats:italic>in vitro<\/jats:italic> evidence that microglia and astrocytes are glutamate suppliers in response to soluble iron overload and oxidative stress, respectively, in sporadic ALS.<\/jats:p>","DOI":"10.1111\/neup.13033","type":"journal-article","created":{"date-parts":[[2025,3,12]],"date-time":"2025-03-12T04:47:24Z","timestamp":1741754844000},"page":"177-201","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Implications for soluble iron accumulation, oxidative stress, and glial glutamate release in motor neuron death associated with sporadic amyotrophic lateral sclerosis"],"prefix":"10.1111","volume":"45","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-7544-5787","authenticated-orcid":false,"given":"Noriyuki","family":"Shibata","sequence":"first","affiliation":[{"name":"Department of Neurology and Internal Medicine Sayama Shojukai 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