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Previous studies have demonstrated that the CX3CR1 receptor plays a crucial role in maintaining an early protective microenvironment after stroke, but whether it persistently influences cognitive dysfunction in the chronic phase requires further investigation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Mouse was used to establish a middle cerebral artery occlusion (MCAO)\/reperfusion model to study PSCI. Cognitive function was assessed by the Morris water maze (MWM) and the novel object recognition test. Neurogenesis was assessed by immunofluorescence staining with Nestin\n                      <jats:sup>+<\/jats:sup>\n                      \/Ki67\n                      <jats:sup>+<\/jats:sup>\n                      and DCX\n                      <jats:sup>+<\/jats:sup>\n                      \/BrdU\n                      <jats:sup>+<\/jats:sup>\n                      double\u2010positive cells. The cerebral damage was monitored by [\n                      <jats:sup>18<\/jats:sup>\n                      F]\u2010DPA\u2010714 positron emission tomography, Nissel, and TTC staining. The pyroptosis was histologically, biochemically, and electron microscopically examined.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Upon MCAO, at 28 to 35\u2009days, CX3CR1 knockout (CX3CR1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      ) mice had better cognitive behavioral performance both in MWM and novel object recognition test than their CX3CR1\n                      <jats:sup>+\/\u2212<\/jats:sup>\n                      counterparts. Upon MCAO, at 7\u2009days, CX3CR1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice increased the numbers of Nestin\n                      <jats:sup>+<\/jats:sup>\n                      \/Ki67\n                      <jats:sup>+<\/jats:sup>\n                      and DCX\n                      <jats:sup>+<\/jats:sup>\n                      \/BrdU\n                      <jats:sup>+<\/jats:sup>\n                      cells, and meanwhile it decreased the protein expression of GSDMD, NLRP3 inflammasome subunit, caspase\u20101, mature IL\u20101\u03b2\/IL\u201018, and p\u2010P65 in the hippocampus as compared with CX3CR1\n                      <jats:sup>+\/\u2212<\/jats:sup>\n                      mice. In addition, CX3CR1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice could reverse infarct volume in the hippocampus region post\u2010stroke.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our study demonstrated that CX3CR1 gene deletion was beneficial to PSCI recovery. The mechanism might lie in inhibited pyroptosis and enhanced neurogenesis. CX3CR1 receptor may serve as a therapeutic target for improving the PSCI.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/cns.14551","type":"journal-article","created":{"date-parts":[[2024,2,8]],"date-time":"2024-02-08T01:33:49Z","timestamp":1707356029000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Absence in\n                    <scp>CX3CR1<\/scp>\n                    receptor signaling promotes post\u2010ischemic stroke cognitive function recovery through suppressed microglial pyroptosis in mice"],"prefix":"10.1111","volume":"30","author":[{"given":"Yangyang","family":"Ge","sequence":"first","affiliation":[{"name":"Department of Anesthesiology, Union Hospital, Tongji Medical College Huazhong University of Science and Technology  Wuhan China"},{"name":"Institute of Anesthesia and Critical Care Medicine, Union Hospital, Tongji Medical College Huazhong University of Science and Technology  Wuhan 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