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
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 sequelae