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(AAO). Multiple factors, including genetic factors, may underlie this variability; however, the specific determinants remain unclear. To identify genes affecting AAO, we have conducted a genome-wide association study in Japanese patients with ALS (discovery cohort: n\u2009=\u20091808; replication cohort: n\u2009=\u2009207). Here, we show that the minor A allele of rs113161727 at the\n                    <jats:italic>ADAM29<\/jats:italic>\n                    -\n                    <jats:italic>GPM6A<\/jats:italic>\n                    locus is associated with a younger AAO in the discovery cohort (effect, -4.27 years; p\u2009=\u20094.60 \u00d7 10\n                    <jats:sup>-8<\/jats:sup>\n                    ); this finding has been confirmed in the replication cohort (p\u2009=\u20090.0068) and meta-analysis (p\u2009=\u20091.08 \u00d7 10\n                    <jats:sup>\u22129<\/jats:sup>\n                    ). Among 65 ALS patients with a\n                    <jats:italic>SOD1<\/jats:italic>\n                    mutation, the AAO has been found to be 10.2 years younger in those with the A allele than in those without it (p\u2009=\u20090.002). This variant correlates with\n                    <jats:italic>GPM6A<\/jats:italic>\n                    upregulation in iPSC-derived motor neurons, suggesting\n                    <jats:italic>GPM6A<\/jats:italic>\n                    as a candidate AAO modifier. Overall, our study highlights the impact of genetic modifiers on ALS heterogeneity and provides a potential target for delaying disease onset.\n                  <\/jats:p>","DOI":"10.1038\/s42003-025-09168-4","type":"journal-article","created":{"date-parts":[[2025,12,5]],"date-time":"2025-12-05T10:03:10Z","timestamp":1764928990000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["A genome-wide association study identifies the GPM6A locus associated with age at onset in 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