{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T16:35:50Z","timestamp":1793378150567,"version":"4.5.0"},"reference-count":89,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"785","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Transl. Med."],"published-print":{"date-parts":[[2025,2,12]]},"abstract":"<jats:p>\n                    Expanded CAG alleles in the huntingtin (\n                    <jats:italic>HTT<\/jats:italic>\n                    ) gene that cause the neurodegenerative disorder Huntington\u2019s disease (HD) are genetically unstable and continue to expand somatically throughout life, driving HD onset and progression. MSH3, a DNA mismatch repair protein, modifies HD onset and progression by driving this somatic CAG repeat expansion process.\n                    <jats:italic>MSH3<\/jats:italic>\n                    is relatively tolerant of loss-of-function variation in humans, making it a potential therapeutic target. Here, we show that an\n                    <jats:italic>MSH3<\/jats:italic>\n                    -targeting antisense oligonucleotide (ASO) effectively engaged with its RNA target in induced pluripotent stem cell (iPSC)\u2013derived striatal neurons obtained from a patient with HD carrying\n                    <jats:italic>125 HTT<\/jats:italic>\n                    CAG repeats (the 125 CAG iPSC line). ASO treatment led to a dose-dependent reduction of MSH3 and subsequent stalling of CAG repeat expansion in these striatal neurons. Bulk RNA sequencing revealed a safe profile for\n                    <jats:italic>MSH3<\/jats:italic>\n                    reduction, even when reduced by &gt;95%. Maximal knockdown of MSH3 also effectively slowed CAG repeat expansion in striatal neurons with an otherwise accelerated expansion rate, derived from the 125 CAG iPSC line where\n                    <jats:italic>FAN1<\/jats:italic>\n                    was knocked out by CRISPR-Cas9 editing. Last, we created a knock-in mouse model expressing the human\n                    <jats:italic>MSH3<\/jats:italic>\n                    gene and demonstrated effective in vivo reduction in human\n                    <jats:italic>MSH3<\/jats:italic>\n                    after ASO treatment. Our study shows that ASO-mediated MSH3 reduction can prevent\n                    <jats:italic>HTT<\/jats:italic>\n                    CAG repeat expansion in HD 125 CAG iPSC\u2013derived striatal neurons, highlighting the therapeutic potential of this approach.\n                  <\/jats:p>","DOI":"10.1126\/scitranslmed.adn4600","type":"journal-article","created":{"date-parts":[[2025,2,12]],"date-time":"2025-02-12T13:59:31Z","timestamp":1739368771000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":60,"title":["Antisense oligonucleotide\u2013mediated MSH3 suppression reduces somatic CAG repeat expansion in Huntington\u2019s disease iPSC\u2013derived striatal neurons"],"prefix":"10.1126","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-0698-9696","authenticated-orcid":true,"given":"Emma L.","family":"Bunting","sequence":"first","affiliation":[{"name":"Huntington\u2019s Disease Centre and Department of 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