2024
Siponimod Attenuates Neuronal Cell Death Triggered by Neuroinflammation via NFκB and Mitochondrial Pathways
Gurrea-Rubio M, Wang Q, Mills E, Wu Q, Pitt D, Tsou P, Fox D, Mao-Draayer Y. Siponimod Attenuates Neuronal Cell Death Triggered by Neuroinflammation via NFκB and Mitochondrial Pathways. International Journal Of Molecular Sciences 2024, 25: 2454. PMID: 38473703, PMCID: PMC10931690, DOI: 10.3390/ijms25052454.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAzetidinesBenzyl CompoundsCell DeathHumansMultiple SclerosisMultiple Sclerosis, Chronic ProgressiveNeuroinflammatory DiseasesNeuroprotective AgentsRatsSphingosine-1-Phosphate ReceptorsTumor Necrosis Factor-alphaConceptsSecondary progressive MSRelapsing-remitting MSCentral nervous systemMultiple sclerosisProgressive MSModulator of sphingosine-1-phosphateCytokine tumor necrosis factor-alphaEffects of siponimodTumor necrosis factor-alphaHeterogeneous clinical courseBouts of inflammationNeuroprotective effectsPreclinical animal modelsAutoimmune demyelinating diseaseNecrosis factor-alphaMitochondrial oxidative phosphorylationHuman induced pluripotent stem cell (iPSC)-derived neuronsSphingosine-1-phosphateCytokine signaling pathwaysClinical courseLive cell analysisProgressive diseaseOral treatmentMitochondrial pathwayFactor-alpha
2022
Toward Precision Phenotyping of Multiple Sclerosis
Pitt D, Lo CH, Gauthier SA, Hickman RA, Longbrake E, Airas LM, Mao-Draayer Y, Riley C, De Jager PL, Wesley S, Boster A, Topalli I, Bagnato F, Mansoor M, Stuve O, Kister I, Pelletier D, Stathopoulos P, Dutta R, Lincoln MR. Toward Precision Phenotyping of Multiple Sclerosis. Neurology Neuroimmunology & Neuroinflammation 2022, 9: e200025. PMID: 36041861, PMCID: PMC9427000, DOI: 10.1212/nxi.0000000000200025.Peer-Reviewed Original ResearchMeSH KeywordsBiomarkersDisease ProgressionHumansInflammationMultiple SclerosisMultiple Sclerosis, Chronic ProgressiveNervous System DiseasesConceptsMultiple sclerosisSecondary progressive multiple sclerosisPathological processesProgressive multiple sclerosisKey pathological processClinical trial designDevelopment of biomarkersPerilesional inflammationNeuroaxonal degenerationMS phenotypeTrial designClinical importancePersonalized careM phenotypeSclerosisPhenotypeRemyelinationInflammationSyndromePrognosticationDegenerationProgressionBiomarkersCare
2013
Iron Is a Sensitive Biomarker for Inflammation in Multiple Sclerosis Lesions
Mehta V, Pei W, Yang G, Li S, Swamy E, Boster A, Schmalbrock P, Pitt D. Iron Is a Sensitive Biomarker for Inflammation in Multiple Sclerosis Lesions. PLOS ONE 2013, 8: e57573. PMID: 23516409, PMCID: PMC3597727, DOI: 10.1371/journal.pone.0057573.Peer-Reviewed Original ResearchMeSH KeywordsAdultBiomarkersBrainHumansInflammationIronMacrophagesMagnetic Resonance ImagingMultiple SclerosisMultiple Sclerosis, Chronic ProgressiveMultiple Sclerosis, Relapsing-RemittingMyelin ProteinsPhagocytosisConceptsMyelin-laden macrophagesMS patientsSecondary progressive MS patientsProgressive MS patientsSecondary progressive MSMultiple sclerosis patientsMacrophages/microgliaWhite matter lesionsHuman macrophage culturesIron-containing macrophagesMultiple sclerosis lesionsImportant clinical informationHuman cultured macrophagesActive relapsingDemyelinating lesionsDisease-relevant processesProgressive MSDemyelinated lesionsSclerosis patientsMultiple sclerosisMatter lesionsM1 polarizationImmunohistochemical examinationMyelin phagocytosisProinflammatory polarization