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These repeats produce dipeptide repeat proteins with poly(PR) being the most toxic one.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We performed a kinome\u2010wide CRISPR\/Cas9 knock\u2010out screen in human induced pluripotent stem cell (iPSC) \u2010derived cortical neurons to identify modifiers of poly(PR) toxicity, and validated the role of candidate modifiers using in vitro, in vivo, and ex\u2010vivo studies.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Knock\u2010down of NIMA\u2010related kinase 6 (NEK6) prevented neuronal toxicity caused by poly(PR). Knock\u2010down of nek6 also ameliorated the poly(PR)\u2010induced axonopathy in zebrafish and NEK6 was aberrantly expressed in <jats:italic>C9orf72<\/jats:italic> patients. Suppression of NEK6 expression and NEK6 activity inhibition rescued axonal transport defects in cortical neurons from <jats:italic>C9orf72<\/jats:italic> patient iPSCs, at least partially by reversing p53\u2010related DNA damage.<\/jats:p><\/jats:sec><jats:sec><jats:title>Discussion<\/jats:title><jats:p>We identified NEK6, which regulates poly(PR)\u2010mediated p53\u2010related DNA damage, as a novel therapeutic target for <jats:italic>C9orf72<\/jats:italic> FTD\/ALS.<\/jats:p><\/jats:sec>","DOI":"10.1002\/alz.12760","type":"journal-article","created":{"date-parts":[[2022,8,22]],"date-time":"2022-08-22T07:00:47Z","timestamp":1661151647000},"page":"1245-1259","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":31,"title":["CRISPR\/Cas9 screen in human iPSC\u2010derived cortical neurons identifies NEK6 as a novel disease modifier of <i>C9orf72<\/i> poly(PR) 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