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dc.contributor.authorStetter, Christian
dc.contributor.authorLopez-Caperuchipi, Simon
dc.contributor.authorHopp-Krämer, Sarah
dc.contributor.authorBieber, Michael
dc.contributor.authorKleinschnitz, Christoph
dc.contributor.authorSirén, Anna-Leena
dc.contributor.authorAlbert-Weißenberger, Christiane
dc.date.accessioned2021-07-01T12:20:36Z
dc.date.available2021-07-01T12:20:36Z
dc.date.issued2021-05-03
dc.identifier.citationJ Mol Sci. 2021 May 3;22(9):4855. doi: 10.3390/ijms22094855.en_US
dc.identifier.pmid34063730
dc.identifier.doi10.3390/ijms22094855
dc.identifier.urihttp://hdl.handle.net/10033/622917
dc.description.abstractBased on recent findings that show that depletion of factor XII (FXII) leads to better posttraumatic neurological recovery, we studied the effect of FXII-deficiency on post-traumatic cognitive and behavioral outcomes in female and male mice. In agreement with our previous findings, neurological deficits on day 7 after weight-drop traumatic brain injury (TBI) were significantly reduced in FXII-/- mice compared to wild type (WT) mice. Also, glycoprotein Ib (GPIb)-positive platelet aggregates were more frequent in brain microvasculature of WT than FXII-/- mice 3 months after TBI. Six weeks after TBI, memory for novel object was significantly reduced in both female and male WT but not in FXII-/- mice compared to sham-operated mice. In the setting of automated home-cage monitoring of socially housed mice in IntelliCages, female WT mice but not FXII-/- mice showed decreased exploration and reacted negatively to reward extinction one month after TBI. Since neuroendocrine stress after TBI might contribute to trauma-induced cognitive dysfunction and negative emotional contrast reactions, we measured peripheral corticosterone levels and the ration of heart, lung, and spleen weight to bodyweight. Three months after TBI, plasma corticosterone levels were significantly suppressed in both female and male WT but not in FXII-/- mice, while the relative heart weight increased in males but not in females of both phenotypes when compared to sham-operated mice. Our results indicate that FXII deficiency is associated with efficient post-traumatic behavioral and neuroendocrine recovery.en_US
dc.language.isoenen_US
dc.publisherMDPIen_US
dc.rightsAttribution 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectCrespi effecten_US
dc.subjectIntelliCageen_US
dc.subjectclosed head injuryen_US
dc.subjectcontact-kinin systemen_US
dc.subjectobject recognition memoryen_US
dc.subjectstressen_US
dc.titleAmelioration of Cognitive and Behavioral Deficits after Traumatic Brain Injury in Coagulation Factor XII Deficient Mice.en_US
dc.typeArticleen_US
dc.identifier.eissn1422-0067
dc.contributor.departmentHIRI, Helmholtz-Institut für RNA-basierte Infektionsforschung, Josef-Shneider Strasse 2, 97080 Würzburg, Germany.en_US
dc.identifier.journalInternational journal of molecular sciencesen_US
dc.source.volume22
dc.source.issue9
refterms.dateFOA2021-07-01T12:20:37Z
dc.source.journaltitleInternational journal of molecular sciences
dc.source.countrySwitzerland


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Attribution 4.0 International
Except where otherwise noted, this item's license is described as Attribution 4.0 International