{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T11:22:52Z","timestamp":1787829772725,"version":"build-2784847793"},"reference-count":86,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T00:00:00Z","timestamp":1787788800000},"content-version":"vor","delay-in-days":238,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100000268","name":"Biotechnology and Biological Sciences Research Council","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000268","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["International Journal of Cell Biology"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:p>\n                    Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterised by motor neuron loss and protein aggregation, commonly driven by mutations in superoxide dismutase 1 (Sod1). Recent evidence implicates gut microbiota\u2013derived metabolites, such as butyrate, in modulating neurodegeneration, but the underlying mechanisms remain unclear. Here, we demonstrate that sodium butyrate (NaB), a histone deacetylase inhibitor and microbial metabolite, ameliorates ALS\u2010related phenotypes in\n                    <jats:italic>C. elegans<\/jats:italic>\n                    and mammalian cell models expressing mutant isoforms of Sod1 linked to ALS. NaB treatment prevented Sod1 aggregation and restored motor function and axonal integrity in transgenic worms overexpressing Sod1\n                    <jats:sup>G85R<\/jats:sup>\n                    . Mechanistically, NaB recapitulated the effects of the pan\u2010HDAC inhibitor trichostatin A, suggesting HDAC inhibition as key to reducing Sod1 aggregation and its downstream effects. Application of NaB or the HDAC inhibitor valproic acid also prevented aggregation of Sod1\n                    <jats:sup>A4V<\/jats:sup>\n                    , Sod1\n                    <jats:sup>G85R<\/jats:sup>\n                    or Sod1\n                    <jats:sup>G37R<\/jats:sup>\n                    in transfected human neuroblastoma cells. These findings support a conserved neuroprotective role for NaB and HDAC inhibitors via their antiaggregation activity. Our findings also verify\n                    <jats:italic>C. elegans<\/jats:italic>\n                    and neuroblastoma cell lines as excellent research tools to explore the mechanisms underlying the antiaggregation action of NaB and HDAC inhibitors, as well as their potential for future therapeutic development.\n                  <\/jats:p>","DOI":"10.1155\/ijcb\/3022967","type":"journal-article","created":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T11:06:59Z","timestamp":1787828819000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The HDAC Inhibitor Butyrate Reduces SOD1 Aggregation and Improves Motor Function in\n                    <i>C. elegans<\/i>\n                    and Cellular Models of ALS"],"prefix":"10.1155","volume":"2026","author":[{"given":"Fiona 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