{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,5]],"date-time":"2026-01-05T19:48:09Z","timestamp":1767642489189,"version":"3.48.0"},"reference-count":46,"publisher":"SAGE Publications","license":[{"start":{"date-parts":[[2025,6,9]],"date-time":"2025-06-09T00:00:00Z","timestamp":1749427200000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2025,6,9]],"date-time":"2025-06-09T00:00:00Z","timestamp":1749427200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"DOI":"10.13039\/100000965","name":"American Federation for Aging Research","doi-asserted-by":"crossref","award":["RAG11482"],"award-info":[{"award-number":["RAG11482"]}],"id":[{"id":"10.13039\/100000965","id-type":"DOI","asserted-by":"crossref"}]},{"name":"the U.S.-Israel Bi-national Science Foundation","award":["2011344"],"award-info":[{"award-number":["2011344"]}]},{"name":"Rekanati Foundation"},{"name":"the Israeli Ministry of Health","award":["3-0000-17856"],"award-info":[{"award-number":["3-0000-17856"]}]},{"DOI":"10.13039\/100000957","name":"the Alzheimer\u2019s Association","doi-asserted-by":"crossref","award":["AARG-16-442861"],"award-info":[{"award-number":["AARG-16-442861"]}],"id":[{"id":"10.13039\/100000957","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Chronic Stress"],"published-print":{"date-parts":[[2025,10]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Up to 25% of stroke survivors develop post-traumatic stress disorder (PTSD) symptoms, yet the predisposing factors remain largely unknown. The C-C-Chemokine receptor-5 gene (CCR5) loss-of-function mutation (LOFM, CCR5-\u039432) has been identified as a protective factor against post-stroke depression. This study investigates whether CCR5-\u039432 also confers protection against post-stroke PTSD, in conjunction with two additional polymorphisms: the 5-HTTLPR in the serotonin transporter gene and the BDNF Val66Met variant.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We conducted a prospective analysis of 432 survivors of first-ever mild-to-moderate ischemic stroke, assessing PTSD symptomatology at 6, 12, and 24 months post-stroke. Genetic screening for CCR5-\u039432 status and PTSD symptom data were available for these participants.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      PTSD was diagnosed in 48 participants (11%) within the first year post-stroke. CCR5-\u039432 carriers exhibited significantly fewer PTSD symptoms at 6, 12, and 24 months compared to non-carriers (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      \u2009&lt;\u2009.001,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      \u2009&lt;\u2009.001,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      \u2009=\u2009.02, respectively), with sustained improvement over time. Multivariate analysis confirmed that CCR5-\u039432 status was independently associated with lower PTSD risk after adjusting for relevant confounders. Furthermore, individuals with a maladaptive coping style who were non-carriers of CCR5-\u039432 exhibited a higher risk of PTSD development (HR\u2009=\u20094.03; 95% CI, 1.95-6.32,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      \u2009&lt;\u2009.001). Carriers of both 5-HTTLPR-L and CCR5-\u039432 had significantly lower PTSD symptoms at 6 and 12 months post-stroke (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      \u2009=\u2009.026,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      \u2009=\u2009.05), as did carriers of both the BDNF Val allele and CCR5-\u039432 at 6 months (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      \u2009=\u2009.022).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our findings suggest that CCR5-\u039432 carriers are less likely to develop PTSD symptoms following stroke, including individuals with pre-existing maladaptive coping styles. These results highlight a potential genetic target for future intervention strategies, with CCR5 blockade emerging as a promising therapeutic avenue for post-stroke PTSD prevention.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/24705470251345245","type":"journal-article","created":{"date-parts":[[2025,6,10]],"date-time":"2025-06-10T02:21:07Z","timestamp":1749522067000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["Post-Stroke PTSD: The Protective Role of CCR5-\u039432 Polymorphism"],"prefix":"10.1177","volume":"9","author":[{"given":"Hen","family":"Hallevi","sequence":"first","affiliation":[{"name":"Tel Aviv Sourasky Medical Center"},{"name":"Tel Aviv University"},{"name":"Tel Aviv University"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Oren","family":"Tene","sequence":"additional","affiliation":[{"name":"Tel Aviv Sourasky Medical Center"},{"name":"Tel Aviv 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