2025
Early beta-blocker exposure and association with brain injury biomarkers following moderate to severe traumatic brain injury: A TRACK-TBI study.
Wongsripuemtet P, Ohnuma T, Temkin N, Barber J, Komisarow J, Manley G, Hatfield J, Treggiari M, Colton K, Sasannejad C, Chaikittisilpa N, Grandhi R, Laskowitz D, Mathew J, Hernandez A, James M, Raghunathan K, Miller J, Vavilala M, Goldstein B, Krishnamoorthy V. Early beta-blocker exposure and association with brain injury biomarkers following moderate to severe traumatic brain injury: A TRACK-TBI study. Journal Of The Intensive Care Society 2025, 17511437251349680. PMID: 40600218, PMCID: PMC12206746, DOI: 10.1177/17511437251349680.Peer-Reviewed Original ResearchNeuron-specific enolase levelsBeta-blocker exposureNeuron-specific enolaseUbiquitin C-terminal hydrolase-L1Beta-blockersC-reactive proteinBrain injury biomarkersIntensive care unitGlial fibrillary acidic proteinBiomarker levelsBB+ groupInjury biomarkersPrimary outcomeTraumatic brain injuryS100 calcium-binding protein BUCH-L1 levelsCalcium-binding protein BInflammatory biomarkers C-reactive proteinPropensity-weighted modelsRetrospective cohort studyPropensity-weighted analysisBiomarkers C-reactive proteinPotential neuroprotective effectsFibrillary acidic proteinRandomized Controlled Trials
2020
Neuroprotective Effects of Lithium in Chemotherapy‐induced Cognitive Impairments
Nguyen L, Fischer T, Ehrlich B. Neuroprotective Effects of Lithium in Chemotherapy‐induced Cognitive Impairments. The FASEB Journal 2020, 34: 1-1. DOI: 10.1096/fasebj.2020.34.s1.00558.Peer-Reviewed Original ResearchCognitive impairmentNeuroprotective effectsChemotherapy-induced cognitive impairmentProtein kinase CPotential neuroprotective effectsGolgi-Cox stainingLife-saving treatmentSpatial memory acquisitionCancer survivorsLast injectionSpine densityCancer patientsNeurological dysfunctionDendritic arborizationIntraperitoneal injectionLithium pretreatmentPaclitaxel injectionMouse modelPaclitaxel treatmentSide effectsCellular deficitsSpecific cognitive functionsNeurodegenerative disordersCognitive functionImpairment
2015
Spermidine ameliorates 3-nitropropionic acid (3-NP)-induced striatal toxicity: Possible role of oxidative stress, neuroinflammation, and neurotransmitters
Jamwal S, Kumar P. Spermidine ameliorates 3-nitropropionic acid (3-NP)-induced striatal toxicity: Possible role of oxidative stress, neuroinflammation, and neurotransmitters. Physiology & Behavior 2015, 155: 180-187. PMID: 26703234, DOI: 10.1016/j.physbeh.2015.12.015.Peer-Reviewed Original ResearchConceptsHuntington's diseaseStriatal toxicityStriatal neurotransmittersRat striatumMotor coordinationPro-inflammatory cytokine levelsOxidative stressPro-inflammatory mediatorsPotential neuroprotective effectsAnti-inflammatory propertiesGood experimental modelConfer neuroprotectionCytokine levelsNeuroinflammatory markersNeuroprotective effectsPresent studyNeurochemical analysisBody weightTherapeutic potentialNeurodegenerative disordersBiochemical parametersExperimental modelDecreased levelsNeurotransmittersSignificant alterationsTriptolide attenuated injury via inhibiting oxidative stress in Amyloid-Beta25–35-treated differentiated PC12 cells
Xu P, Wang H, Li Z, Yang Z. Triptolide attenuated injury via inhibiting oxidative stress in Amyloid-Beta25–35-treated differentiated PC12 cells. Life Sciences 2015, 145: 19-26. PMID: 26679104, DOI: 10.1016/j.lfs.2015.12.018.Peer-Reviewed Original ResearchConceptsDifferentiated PC12 cellsAβ25-35Alzheimer's diseaseOxidative stressPC12 cellsAβ25-35-induced apoptosisTreatment of ADReactive oxygen speciesPotential neuroprotective effectsEffects of triptolideAβ25-35-induced cytotoxicityDecreased oxidative stressSuperoxide dismutaseProtective functionNeuroprotective effectsImmunohistochemical stainingProtective effectResults of MTTAmyloid betaHerb TripterygiumNervous systemAbnormal depositionCytometry assaysWestern blotTriptolide
2013
UCP2 overexpression worsens mitochondrial dysfunction and accelerates disease progression in a mouse model of amyotrophic lateral sclerosis
Peixoto PM, Kim HJ, Sider B, Starkov A, Horvath TL, Manfredi G. UCP2 overexpression worsens mitochondrial dysfunction and accelerates disease progression in a mouse model of amyotrophic lateral sclerosis. Molecular And Cellular Neuroscience 2013, 57: 104-110. PMID: 24141050, PMCID: PMC3891658, DOI: 10.1016/j.mcn.2013.10.002.Peer-Reviewed Original ResearchConceptsAmyotrophic lateral sclerosisDouble transgenic miceFamilial amyotrophic lateral sclerosisMouse modelLateral sclerosisMitochondrial dysfunctionTransgenic miceMutant SOD1 mouse modelHuman UCP2Brain mitochondriaSOD1 mutant miceUCP2 overexpressionPotential neuroprotective effectsProtection of neuronsSOD1 mouse modelCentral nervous systemReactive oxygen species productionDisease courseG93A miceNeuroprotective effectsNeuroprotective roleFree radical generationDisease progressionOxygen species productionInjury paradigms
2008
18 MULTIPLE SCLEROSIS: REMYELINATION
KOCSIS J, SASAKI M, LANKFORD K, RADTKE C. 18 MULTIPLE SCLEROSIS: REMYELINATION. 2008, 413-435. DOI: 10.1016/b978-012373994-0.50020-8.Peer-Reviewed Original ResearchMyelin-forming cellsMultiple sclerosisConduction abnormalitiesPotential neuroprotective effectsProminent pathological featurePeripheral nervous systemEndogenous progenitor cellsPotassium channel distributionRemyelinated axonsIon channel organizationDemyelinated lesionsNeuroprotective effectsAxonal transectionPathological featuresFunctional deficitsMyelin repairAxonal repairMyelin resultsNervous systemImpulse conductionProgenitor cellsRemyelinationSclerosisTransectionAbnormalities
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