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Previous studies have suggested psoriatic patients are at higher risk of MS; however, causal relationships between the two conditions remain unclear. Through epidemiology and genetics, we provide a comprehensive understanding of the relationship, and share molecular factors between psoriasis and MS.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We used logistic regression, trans\u2010disease meta\u2010analysis and Mendelian randomization. Medical claims data were included from 30 million patients, including 141,544 with MS and 742,919 with psoriasis. We used genome\u2010wide association study summary statistics from 11,024 psoriatic, 14,802 MS cases, and 43,039 controls for trans\u2010disease meta\u2010analysis, with additional summary statistics from 5 million individuals for Mendelian randomization.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Psoriatic patients have a significantly higher risk of MS (4,637 patients with both diseases; odds ratio [OR] 1.07, <jats:italic>p<\/jats:italic>\u2009=\u20091.2\u2009\u00d7\u200910<jats:sup>\u22125<\/jats:sup>) after controlling for potential confounders. Using inverse variance and equally weighted trans\u2010disease meta\u2010analysis, we revealed &gt;20 shared and opposing (direction of effect) genetic loci outside the major histocompatibility complex that showed significant genetic colocalization (in COLOC and COLOC\u2010SuSiE v5.1.0). Co\u2010expression analysis of genes from these loci further identified distinct clusters that were enriched among pathways for interleukin\u201017\/tumor necrosis factor\u2010\u03b1 (OR &gt;39, <jats:italic>p<\/jats:italic>\u2009&lt;\u20091.6\u2009\u00d7\u200910<jats:sup>\u22123<\/jats:sup>) and <jats:styled-content style=\"fixed-case\">Janus kinase\u2013signal transducers and activators of transcription<\/jats:styled-content> (OR 35, <jats:italic>p<\/jats:italic>\u2009=\u20091.1\u2009\u00d7\u200910<jats:sup>\u22125<\/jats:sup>), including genes, such as <jats:italic>TNFAIP3<\/jats:italic>, <jats:italic>TYK2<\/jats:italic>, and <jats:italic>TNFRSF1A<\/jats:italic>. Mendelian randomization found psoriasis as an exposure has a significant causal effect on MS (OR 1.04, <jats:italic>p<\/jats:italic>\u2009=\u20095.8\u2009\u00d7\u200910<jats:sup>\u22123<\/jats:sup>), independent of type\u20091 diabetes (OR 1.05, <jats:italic>p<\/jats:italic>\u2009=\u20094.3\u2009\u00d7\u200910<jats:sup>\u22127<\/jats:sup>), type\u20092 diabetes (OR 1.08, <jats:italic>p<\/jats:italic>\u2009=\u20092.3\u2009\u00d7\u200910<jats:sup>\u22123<\/jats:sup>), inflammatory bowel disease (OR 1.11, <jats:italic>p<\/jats:italic>\u2009=\u20091.6\u2009\u00d7\u200910<jats:sup>\u221211<\/jats:sup>), and vitamin D level (OR 0.75, <jats:italic>p<\/jats:italic>\u2009=\u20099.4\u2009\u00d7\u200910<jats:sup>\u22123<\/jats:sup>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p>By investigating the shared genetics of psoriasis and MS, along with their modifiable risk factors, our findings will advance innovations in treatment for patients suffering from comorbidities. ANN NEUROL 2023;94:384\u2013397<\/jats:p><\/jats:sec>","DOI":"10.1002\/ana.26672","type":"journal-article","created":{"date-parts":[[2023,5,2]],"date-time":"2023-05-02T04:11:51Z","timestamp":1683000711000},"page":"384-397","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Shared Genetic Risk Factors for <scp>Multiple Sclerosis<\/scp>\/Psoriasis Suggest Involvement of <scp>Interleukin\u201017<\/scp> and <scp>Janus Kinase\u2013Signal Transducers and Activators of Transcription<\/scp> Signaling"],"prefix":"10.1002","volume":"94","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6174-9002","authenticated-orcid":false,"given":"Matthew T.","family":"Patrick","sequence":"first","affiliation":[{"name":"Department of Dermatology University of Michigan Medical School  Ann Arbor MI USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rajan 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