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 ResearchConceptsSecondary 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
2014
IFN-β alters neurotrophic factor expression in T cells isolated from multiple sclerosis patients - implication of novel neurotensin/NTSR1 pathway in neuroprotection.
Soltys J, Knight J, Scharf E, Pitt D, Mao-Draayer Y. IFN-β alters neurotrophic factor expression in T cells isolated from multiple sclerosis patients - implication of novel neurotensin/NTSR1 pathway in neuroprotection. American Journal Of Translational Research 2014, 6: 312-9. PMID: 24936223, PMCID: PMC4058312.Peer-Reviewed Original ResearchT cellsMultiple sclerosisNeurotrophin receptorActive demyelinating lesionsNeurotrophic factor expressionCytokine expression patternsHigh-affinity receptor 1Mechanism of actionDemyelinating lesionsMS pathogenesisRRMS patientsNeurotrophin productionNeuroprotective effectsNeurotrophin expressionNeuroprotective capabilitiesStem/progenitor cell survivalProgenitor cell survivalDisease pathogenesisReceptor 1Factor expressionIFNPotent inducerSpecific cell populationsCell populationsSclerosis