{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,17]],"date-time":"2026-06-17T15:04:59Z","timestamp":1781708699601,"version":"3.54.5"},"reference-count":56,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circ: Genomic and Precision Medicine"],"published-print":{"date-parts":[[2025,6]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>The genetic risk of intracranial aneurysm (IA) development has been ascribed to the genetic risk of smoking exposure and hypertension. The relationship of IA to other cardiovascular traits and the contribution of IA risk loci to aberrant gene programs within cerebrovascular cell types remains unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>We performed a genome-wide association study in the Million Veteran Program and Finnish cohort study testing association of roughly 25 million DNA variants with unruptured IA (4694 cases and 877\u2005091 controls) in individuals of European, African, and Hispanic ancestries. Meta-analysis with publicly available summary statistics generated a final cohort of 15 438 cases and 1\u2005183\u2005973 controls. We constructed a cerebrovascular single-nuclear RNA sequencing data set and integrated IA summary statistics to prioritize candidate causal cell types. We constructed a polygenic risk score to identify patients at risk of developing IA.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      We identified 5 novel associations with IA, increasing the number of known susceptibility loci to 22. At these susceptibility loci, we prioritized 17 candidate causal genes. We found a significant positive genetic correlation of IA with coronary artery disease and abdominal aortic aneurysm. Integration of an IA gene set with cerebrovascular single-nuclear RNA sequencing data revealed a significant association with pericytes and smooth muscle cells. Finally, a polygenic risk score was significantly associated with IA across European (odds ratio, 1.87 [95% CI, 1.61\u20132.17];\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =8.8\u00d710\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:sup>17<\/jats:sup>\n                      ), African (odds ratio, 1.62 [95% CI, 1.19\u20132.15];\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =1.2\u00d710\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:sup>3<\/jats:sup>\n                      ), and Hispanic (odds ratio, 2.28 [95% CI, 1.47\u20133.38];\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =1.0\u00d710\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:sup>4<\/jats:sup>\n                      ) ancestries.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>Here, we identify 5 novel loci associated with IA. Integration of summary statistics with cerebrovascular single-nuclear RNA sequencing reveals an association of cell types involved in matrix production. We validated a polygenic risk score that predicts IA, controlling for demographic variables including smoking status and blood pressure. Our findings suggest that a deficit in matrix production may drive IA pathogenesis independent of hypertension and smoking.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circgen.123.004626","type":"journal-article","created":{"date-parts":[[2025,4,21]],"date-time":"2025-04-21T05:00:16Z","timestamp":1745211616000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":4,"title":["Dissecting the Genetic Architecture of Intracranial Aneurysms"],"prefix":"10.1161","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8893-2413","authenticated-orcid":true,"given":"Shaunak S.","family":"Adkar","sequence":"first","affiliation":[{"name":"Division of Vascular Surgery, Department of Surgery (S.S.A., J.C., S. Sorondo, N.J.L., D.K.), Stanford University School of Medicine, Palo Alto, CA."},{"name":"Stanford Cardiovascular Institute, Stanford University, CA (S.S.A., S.B., J.C., S. Sorondo. 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(J.L.)."},{"name":"Epidemiology, School of Medicine, The University of Utah, Salt Lake City (J.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryan B.","family":"Choi","sequence":"additional","affiliation":[{"name":"Stanford University School of Medicine, Palo Alto, CA (R.B.C.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tanmoy","family":"Roychowdhury","sequence":"additional","affiliation":[{"name":"Department of Biology and Koita Centre for Digital Health, Trivedi School of Biosciences, Ashoka University, Sonepat, India (T.R.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0915-2222","authenticated-orcid":true,"given":"Renae L.","family":"Judy","sequence":"additional","affiliation":[{"name":"Department of Surgery (R.L.J.), University of Pennsylvania Perelman School of Medicine, Philadelphia."},{"name":"Research (R.L.J.), Corporal Michael J. 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