2023
Effects of anti‐tau immunotherapy on reactive microgliosis, cerebral endotheliopathy, and cognitive function in an experimental model of cerebral malaria
Ndunge O, Shikani H, Dai M, Freeman B, Desruisseaux M. Effects of anti‐tau immunotherapy on reactive microgliosis, cerebral endotheliopathy, and cognitive function in an experimental model of cerebral malaria. Journal Of Neurochemistry 2023, 167: 441-460. PMID: 37814468, PMCID: PMC10596299, DOI: 10.1111/jnc.15972.Peer-Reviewed Original ResearchConceptsNeural cell injuryCerebral malariaExperimental CMCell injuryUninfected micePHF-1Cell activationNeurodegenerative diseasesAbnormal regulationExperimental modelAnti-tau immunotherapyTau-targeting therapiesExperimental cerebral malariaGlial cell activationPlasmodium berghei ANKAPlasmodium berghei NK65Abnormal tau phosphorylationSubsequent neurocognitive impairmentSignificant memory impairmentNeural cell damageMicrovascular congestionPbA infectionInflammatory markersBerghei ANKANeurological deficits
2016
Endothelin-1 Treatment Induces an Experimental Cerebral Malaria–Like Syndrome in C57BL/6 Mice Infected with Plasmodium berghei NK65
Martins YC, Freeman BD, Ndunge O, Weiss LM, Tanowitz HB, Desruisseaux MS. Endothelin-1 Treatment Induces an Experimental Cerebral Malaria–Like Syndrome in C57BL/6 Mice Infected with Plasmodium berghei NK65. American Journal Of Pathology 2016, 186: 2957-2969. PMID: 27640146, PMCID: PMC5222963, DOI: 10.1016/j.ajpath.2016.07.020.Peer-Reviewed Original ResearchConceptsExperimental cerebral malariaEndothelin-1ET-1 treatmentC57BL/6 miceBerghei NK65Pathogenesis of ECMBlood-brain barrier leakagePlasmodium berghei ANKA infectionBlood-brain barrier permeabilitySevere malarial diseasePlasmodium berghei ANKABerghei ANKA infectionP. berghei NK65Plasmodium berghei NK65Functional capillary densityEndothelin-1 treatmentCerebral malariaMicrovascular alterationsANKA infectionBerghei ANKARed blood cellsVascular dysfunctionCerebral microvasculatureNeurological signsBarrier leakage
2013
Alterations in Glucose Homeostasis in a Murine Model of Chagas Disease
Nagajyothi F, Kuliawat R, Kusminski CM, Machado FS, Desruisseaux MS, Zhao D, Schwartz GJ, Huang H, Albanese C, Lisanti MP, Singh R, Li F, Weiss LM, Factor SM, Pessin JE, Scherer PE, Tanowitz HB. Alterations in Glucose Homeostasis in a Murine Model of Chagas Disease. American Journal Of Pathology 2013, 182: 886-894. PMID: 23321322, PMCID: PMC3586686, DOI: 10.1016/j.ajpath.2012.11.027.Peer-Reviewed Original ResearchConceptsPancreatic β-cellsChagas diseaseΒ-cellsGlucose-6-phosphatase mRNAChronic phaseInsulin levelsCruzi infectionGlucose homeostasisPlasma membraneInsulin granulesΒ-cell dysfunctionTrypanosoma cruziHost glucose homeostasisT. cruzi infectionElevated glucagon levelsΑ-cell functionAdrenergic receptor agonistDiminished insulin responsePancreatic islet architectureReduced insulinMice resultsAcute infectionCardiac dysfunctionGlucagon levelsPancreatic inflammation
2012
Altered Regulation of Akt Signaling with Murine Cerebral Malaria, Effects on Long-Term Neuro-Cognitive Function, Restoration with Lithium Treatment
Dai M, Freeman B, Shikani HJ, Bruno FP, Collado JE, Macias R, Reznik SE, Davies P, Spray DC, Tanowitz HB, Weiss LM, Desruisseaux MS. Altered Regulation of Akt Signaling with Murine Cerebral Malaria, Effects on Long-Term Neuro-Cognitive Function, Restoration with Lithium Treatment. PLOS ONE 2012, 7: e44117. PMID: 23082110, PMCID: PMC3474787, DOI: 10.1371/journal.pone.0044117.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsChloroquineCognitionFemaleFluorescent Antibody TechniqueGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaImmunoblottingLithiumMalaria, CerebralMiceMice, Inbred C57BLMotor ActivityParasitemiaPhosphorylationProto-Oncogene Proteins c-aktSignal TransductionTau ProteinsConceptsExperimental cerebral malaria modelMotor coordination deficitsAnti-parasitic treatmentChloroquine treatmentCoordination deficitsUninfected controlsLong-term neurological sequelaeCerebral malaria modelCerebral malaria patientsCognitive impairment persistsLong-term neuroMurine cerebral malariaNegative neurological outcomesPbA-infected micePlasmodium berghei ANKABrains of miceP. berghei NK65Adjunctive therapeutic targetManagement of CMAkt activationAkt/GSK3βVisual memory impairmentECM miceNeurological outcomeNeurological sequelaeResponse of Adipose Tissue to Early Infection With Trypanosoma cruzi (Brazil Strain)
Nagajyothi F, Desruisseaux MS, Machado FS, Upadhya R, Zhao D, Schwartz GJ, Teixeira MM, Albanese C, Lisanti MP, Chua SC, Weiss LM, Scherer PE, Tanowitz HB. Response of Adipose Tissue to Early Infection With Trypanosoma cruzi (Brazil Strain). The Journal Of Infectious Diseases 2012, 205: 830-840. PMID: 22293433, PMCID: PMC3274374, DOI: 10.1093/infdis/jir840.Peer-Reviewed Original ResearchMeSH KeywordsAdipocytesAdiponectinAdipose Tissue, BrownAdipose Tissue, WhiteAnimalsChagas DiseaseChemokinesCytokinesI-kappa B KinaseMaleMiceMitogen-Activated Protein KinasesNF-kappa BPPAR gammaReceptors, ChemokineRNA, MessengerSignal TransductionToll-Like Receptor 4Toll-Like Receptor 9Trypanosoma cruziConceptsWhite adipose tissueBrown adipose tissueAdipose tissueCruzi infectionNuclear factor kappa B (NF-κB) levelsToll-like receptor 4Peroxisome proliferator-activated receptor γProliferator-activated receptor γMRNA levelsTrypanosoma cruzi infectionMessenger RNA levelsReceptor 4Adipocyte sizeFat massHigher parasite loadsReceptor γEarly infectionExpression of componentsInfectionB levelsLipid accumulationRNA levelsParasite loadEarly targetProtein kinase pathway