{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T13:42:58Z","timestamp":1793281378721,"version":"4.5.0"},"reference-count":93,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T00:00:00Z","timestamp":1783555200000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["23POST1026423"],"award-info":[{"award-number":["23POST1026423"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["23CDA1055341"],"award-info":[{"award-number":["23CDA1055341"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["26PRE1560109"],"award-info":[{"award-number":["26PRE1560109"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["CNS Neurosci Ther"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Mechanical thrombectomy (MT) has become a cornerstone therapy for acute ischemic stroke (AIS) caused by large\u2010vessel occlusion; however, incomplete microvascular reperfusion and blood\u2013brain barrier (BBB) disruption frequently limit its clinical benefit. Emerging evidence implicates neutrophil\u2010driven thrombo\u2010inflammation, particularly neutrophil extracellular trap (NET)\u2013mediated microvascular obstruction, as a key mechanism underlying post\u2010reperfusion hypoperfusion and secondary neurovascular injury. Colchicine, an FDA\u2010approved microtubule inhibitor, potently suppresses neutrophil effector functions with a favorable safety profile, making it a promising adjunct to ischemia\u2013reperfusion.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Using a transient middle cerebral artery occlusion (tMCAO) mouse model of ischemia\u2013reperfusion, colchicine (0.8\u2009mg\/kg, intraperitoneal) was administered at reperfusion. We assessed circulating neutrophil response and activation, neutrophil F\u2010actin polymerization, NET formation, microvascular fibrin(ogen) deposition, cerebral blood flow, leukocyte brain infiltration, BBB integrity, and neuroinflammation at acute and subacute time points. Whole\u2010blood phagocytosis and bone marrow cellularity were examined at Day 3 after tMCAO. Neutrophil depletion was achieved using an anti\u2010Ly6G antibody. Long\u2010term neurological outcomes and brain tissue loss were evaluated up to 14\u2009days after tMCAO.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Colchicine administration at reperfusion significantly blunted early neutrophil increase and activation, inhibited neutrophil F\u2010actin polymerization, and suppressed intravascular NET formation and microvascular fibrin(ogen) deposition in tMCAO mice. It also improved cerebral blood flow, reduced leukocyte brain infiltration, attenuated BBB disruption, and decreased infarct size. Importantly, colchicine\u2010treated mice exhibited sustained improvements in sensorimotor and cognitive function and reduced chronic brain tissue loss. Notably, colchicine did not exacerbate post\u2010stroke immunosuppression, and its neuroprotective effects were abolished by neutrophil depletion.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Colchicine administered at reperfusion suppresses neutrophil\u2010driven thrombo\u2010inflammation, preserves BBB integrity, and improves cerebral blood flow, resulting in reduced ischemic brain injury and long\u2010term neurological deficits after ischemic stroke. These findings suggest colchicine might be developed as a potential adjunctive therapy to limit reperfusion\u2010associated microvascular dysfunction and neurovascular injury.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cns.70922","type":"journal-article","created":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T21:22:26Z","timestamp":1783632146000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Colchicine as an Adjunctive Therapy to Improve Ischemic Stroke Reperfusion Outcomes in Mice"],"prefix":"10.1002","volume":"32","author":[{"ORCID":"https:\/\/orcid.org\/0009-0001-7259-6654","authenticated-orcid":false,"given":"Danni","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Neurology, Tianjin Neurological Institute Tianjin Medical University General Hospital  Tianjin China"},{"name":"Department of Neurosurgery and Neurology, Clinical Neuroscience Research Center Tulane 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