grant

Repetitive Mild TBI and Physiological Stress as Catalysts for Chronic Neurovascular Dysfunction

Organization UNIVERSITY OF KENTUCKYLocation LEXINGTON, UNITED STATESPosted 1 Feb 2026Deadline 31 Jan 2028
NIHUS FederalResearch GrantFY2026(TNF)-αAcuteAffectAffective DisordersAnti-InflammatoriesAnti-Inflammatory AgentsAnti-inflammatoryAnxietyArmed Forces PersonnelAstroproteinAutomobile DrivingB cell differentiation factorB cell stimulating factor 2B-Cell Differentiation FactorB-Cell Differentiation Factor-2B-Cell Stimulatory Factor-2BBB permeabilizationBBB permeableBCDFBSF-2BSF2Behavior DisordersBehavioralBehavioral SymptomsBeta Proprotein Interleukin 1Blood VesselsBlood capillariesBody TissuesBrainBrain InflammationBrain Nervous SystemBrain TraumaBrain VascularCCL2CCL2 geneCD106CD106 AntigensCD54 AntigensCXCL1CXCL1 geneCachectinCerebrovascular systemCerebrumChemokine, CC Motif, Ligand 2ChronicChronic DiseaseChronic IllnessCircadian RhythmsClinical TrialsCognitiveCognitive DisturbanceCognitive ImpairmentCognitive declineCognitive function abnormalDevicesDiffuseDiseaseDisease ProgressionDisorderDisturbance in cognitionDrugsDysfunctionEncephalitisEncephalonEnvironmental FactorEnvironmental Risk FactorEvaluationExperimental ModelsExtravasationFemaleFunctional disorderGFA-ProteinGFAPGRO1GROAGene TranscriptionGenesGenetic TranscriptionGlial Fibrillary Acid ProteinGlial Fibrillary Acidic ProteinGlial Intermediate Filament ProteinHPGFHepatocyte-Stimulating FactorHourHumanHybridoma Growth FactorICAM-1IFN-beta 2IFNB2IL-1 betaIL-1 βIL-1-bIL-1βIL-6IL1-BetaIL1-βIL1B ProteinIL1F2IL1βIL6 ProteinINCAM-110ImageImmunoblottingImpaired cognitionIndividualInducible Cell Adhesion Molecule 110InflammationInjuryIntercellular adhesion molecule 1Interleukin 1betaInterleukin-1 betaInterleukin-1βInterleukin-6InterventionLaboratoriesLaser Speckle ImagingLeakageLesionLifeLightLinkLong-Term EffectsMCAFMCP-1MCP1MGI-2MGSAMTBIMacrophage-Derived TNFMasksMeasurementMeasuresMediatingMedicationMeningesMiceMice MammalsMilitaryMilitary PersonnelModelingModern ManMolecularMonocyte Chemoattractant Protein-1Monocyte Chemotactic Protein-1Monocyte Chemotactic and Activating FactorMonocyte Chemotactic and Activating ProteinMonocyte Chemotactive and Activating FactorMonocyte Secretory Protein JEMonocyte-Derived TNFMood DisordersMurineMusMyeloid Differentiation-Inducing ProteinNerve DegenerationNeuron DegenerationNeurovascular dysfunctionNyctohemeral RhythmOccluding JunctionsOralOutcomePainPainfulPathologicPathologyPatternPerfusionPersonsPharmaceutical PreparationsPhasePhase 1/2 trialPhase I/II TrialPhotoradiationPhysiologicPhysiologicalPhysiologyPhysiopathologyPlasmacytoma Growth FactorPollutionPopulationPreinterleukin 1 BetaProceduresProductionProteinsRNA ExpressionRecoveryRodent ModelRoleSCYA2SCYB1SafetyScheduleSecondary toShapesSleep ApneaSleep Apnea SyndromesSleep FragmentationsSleep HypopneaSleep disturbancesSleep-Disordered BreathingSmall Inducible Cytokine A2SpecificitySpillageStressSymptomsTNFTNF ATNF AlphaTNF geneTNF-αTNFATNFαTestingTherapeuticTherapeutic InterventionTight JunctionsTimeTissuesTracerTranscriptionTraumatic Brain InjuryTraumatic encephalopathyTreatment PeriodTumor Necrosis FactorTumor Necrosis Factor-alphaTwenty-Four Hour RhythmVCAMVCAM-1Vascular Cell Adhesion MoleculeVascular Cell Adhesion Molecule-1Vascular DiseasesVascular DisorderWestern BlottingWestern ImmunoblottingWorkZonula Occludensaberrant sleepaxon damageaxon injuryaxonal damageaxonal injurybehavioral disorderblood vessel disorderblood vessels in the brainblood-brain barrier permeabilizationblood-brain barrier permeablebloodbrain barrier permeabilizationbloodbrain barrier permeablebrain blood vesselsbrain vasculaturecapillarycatalystcerebralcerebral blood vesselcerebral vascularcerebral vasculaturecerebro-vascularcerebrovascularcerebrovascular vesselscerebrovasculaturechronic disorderchronic traumatic encephalopathycircadian processcircadian rhythmicitycognitive dysfunctioncognitive losscytokinedaily biorhythmdesigndesigningdigital pathologydisrupted sleepdisturbed sleepdrivingdrug/agentenvironmental riskenvironmental stressesenvironmental stressorglial activationglial cell activationhyper-phosphorylated tauhyperphosphorylated tauimagingimpaired sleepimproved outcomeinjuriesinjury to the vasculatureinsightinstrumentinterferon beta 2intervention therapyirregular sleeplaser speckle contrast imagingmalemeningemild TBImild brain traumamild traumatic brain injurymilitary injurymilitary populationmouse modelmurine modelneural degenerationneural inflammationneuro-vascularneuro-vascular couplingneuro-vascular unitneurodegenerationneurodegenerativeneuroinflammationneuroinflammatoryneurological degenerationneuronal degenerationneuropathologicneuropathologicalneuropathologyneurovascularneurovascular abnormalityneurovascular couplingneurovascular dysregulationneurovascular impairmentneurovascular pathologyneurovascular unitneurovasculopathyoccludinpathophysiologypharmacologicphysiologic stressesphysiologic stressorphysiological stressespre-clinical studypreclinical studypreventpreventingprotein blottingresponsesleep disruptionsleep dysregulationsleep-related breathing disordersleep/wake disruptionsleep/wake disturbancesocial rolestressortooltranslational frameworktraumatic brain damagetreatment daystreatment durationvascularvascular dysfunctionvascular inflammationvascular injuryvasculopathy
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Project Summary:
Traumatic brain injury (TBI) causes acute neurovascular dysfunction and is associated with long-term

behavioral, cognitive, and neurodegenerative changes that can emerge after initial recovery, yet the

mechanisms underlying this variable latent period remain poorly understood. During this period, secondary

physiological stressors…

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Repetitive Mild TBI and Physiological Stress as Catalysts for Chronic Neurovascular Dysfunction — UNIVERSITY OF KENTUCKY | Dev Procure