2021
Pioglitazone transiently stimulates paraoxonase-2 expression in male nonhuman primate brain: Implications for sex-specific therapeutics in neurodegenerative disorders
Blackburn JK, Jamwal S, Wang W, Elsworth JD. Pioglitazone transiently stimulates paraoxonase-2 expression in male nonhuman primate brain: Implications for sex-specific therapeutics in neurodegenerative disorders. Neurochemistry International 2021, 152: 105222. PMID: 34767873, PMCID: PMC8712400, DOI: 10.1016/j.neuint.2021.105222.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAryldialkylphosphataseBrainFemaleMitochondriaNeurodegenerative DiseasesNeuroprotective AgentsOxidative StressPioglitazonePrimatesSex FactorsConceptsPON2 expressionParkinson's diseaseParaoxonase 2Male African green monkeysShort-term animal modelsOxidative stressPeroxisome proliferator-activated receptor gammaEffect of pioglitazoneWeeks of treatmentProliferator-activated receptor gammaNonhuman primate brainParaoxonase-2 expressionRegion-dependent expressionSex-specific therapeuticsAnti-diabetic drug pioglitazoneAfrican green monkeysDorsolateral prefrontal cortexOral pioglitazonePreclinical evidenceSubstantia nigraClinical trialsPON2 mRNAAnimal modelsPioglitazonePrimate brainNeuroprotection through G-CSF: recent advances and future viewpoints
Rahi V, Jamwal S, Kumar P. Neuroprotection through G-CSF: recent advances and future viewpoints. Pharmacological Reports 2021, 73: 372-385. PMID: 33389706, DOI: 10.1007/s43440-020-00201-3.Peer-Reviewed Original ResearchConceptsGranulocyte-colony stimulating factorNeutrophilic granulocyte lineageNumerous cell typesJAK/STATG-CSF receptorPI3K/AktInhibition of apoptosisTransduction pathwaysHaemopoietic stem cellsMAP kinaseNeuronal differentiationHematopoietic stemCell typesGranulocyte lineageNeurological disordersStem cellsProgenitor cellsRecent pre-clinical studiesHematopoietic growth factorsAttractive targetChemotherapy-associated neutropeniaStimulation of neurogenesisObserved neuroprotective effectsDifferentiationPre-clinical studies
2019
Therapeutic Potential of Agonists and Antagonists of A1, A2a, A2b and A3 Adenosine Receptors.
Jamwal S, Mittal A, Kumar P, Alhayani DM, Al-Aboudi A. Therapeutic Potential of Agonists and Antagonists of A1, A2a, A2b and A3 Adenosine Receptors. Current Pharmaceutical Design 2019, 25: 2892-2905. PMID: 31333104, DOI: 10.2174/1381612825666190716112319.Peer-Reviewed Original ResearchConceptsCentral nervous systemNervous systemFast excitatory postsynaptic currentsCerebral blood flowExcitatory postsynaptic currentsPeripheral nervous systemAntagonists of A1Pharmacology of adenosineA3 adenosine receptorAutonomic gangliaPostsynaptic currentsReceptor agonistMetabolic dysfunctionBlood flowNeuronal activityOcular diseasesSynaptic terminalsTherapeutic strategiesAdenosine receptorsTherapeutic potentialChemical transmissionATP actsExtracellular concentrationReceptors vizNerve signals
2016
Sertraline and venlafaxine improves motor performance and neurobehavioral deficit in quinolinic acid induced Huntington’s like symptoms in rats: Possible neurotransmitters modulation
Gill JS, Jamwal S, Kumar P, Deshmukh R. Sertraline and venlafaxine improves motor performance and neurobehavioral deficit in quinolinic acid induced Huntington’s like symptoms in rats: Possible neurotransmitters modulation. Pharmacological Reports 2016, 69: 306-313. PMID: 28178592, DOI: 10.1016/j.pharep.2016.11.008.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCorpus StriatumDisease Models, AnimalGamma-Aminobutyric AcidGlutamic AcidHuntington DiseaseInterleukin-1betaInterleukin-6Lipid PeroxidationMaleMotor ActivityNeuroprotective AgentsNeurotransmitter AgentsOxidative StressQuinolinic AcidRatsRats, WistarRotarod Performance TestSertralineTumor Necrosis Factor-alphaVenlafaxine HydrochlorideConceptsMotor performanceQuinolinic acidAvailable drugsPro-inflammatory cytokine levelsNumerous neuroprotective propertiesAnti-inflammatory propertiesGrip strength testProgressive neurodegenerative disorderBDNF levelsCytokine levelsSymptomatic reliefNeuroprotective effectsRotarod testMonoamine levelsNeuroprotective propertiesStriatal atrophyNeurobehavioral deficitsNeurotransmitter levelsNeurotransmitter modulationGlutamatergic signalingRat striatumNeurochemical analysisBody weightDay 22Neurochemical levelsL-theanine, a Component of Green Tea Prevents 3-Nitropropionic Acid (3-NP)-Induced Striatal Toxicity by Modulating Nitric Oxide Pathway
Jamwal S, Kumar P. L-theanine, a Component of Green Tea Prevents 3-Nitropropionic Acid (3-NP)-Induced Striatal Toxicity by Modulating Nitric Oxide Pathway. Molecular Neurobiology 2016, 54: 2327-2337. PMID: 26957301, DOI: 10.1007/s12035-016-9822-5.Peer-Reviewed Original ResearchConceptsHuntington's diseaseStriatal toxicityL-NAMENeuroprotective potentialConcurrent treatmentProtective effectBody weightL-arginineL-theanineGABAergic medium spiny neuronsGreen tea preventsStriatal neurotransmitter levelsPro-inflammatory mediatorsPro-inflammatory cytokinesNitric oxide pathwayBlood-brain barrierMedium spiny neuronsNitric oxide productionL-theanine treatmentNeurotransmitter alterationsOxide pathwayBrain barrierSpiny neuronsNeurotransmitter levelsRat striatum
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 alterationsAntidepressants for neuroprotection in Huntington's disease: A review
Jamwal S, Kumar P. Antidepressants for neuroprotection in Huntington's disease: A review. European Journal Of Pharmacology 2015, 769: 33-42. PMID: 26511378, DOI: 10.1016/j.ejphar.2015.10.033.Peer-Reviewed Original ResearchConceptsHuntingtin proteinHuntington's diseaseMAPK/ERK signalingBrain-derived neurotrophic factor (BDNF) productionBDNF/TrkB pathwayProgression of HDDifferent neuroprotective mechanismsPrincipal neuropathological hallmarksUse of antidepressantsNeurotrophic factor productionCortical projection neuronsMutant huntingtin proteinCellular functionsPolyglutamine stretchMolecular mechanismsNH2 terminusERK signalingTrkB pathwayPreclinical evidenceNeuroprotective effectsNeuroprotective mechanismsCommon symptomsProjection neuronsAvailable treatmentsDisease progressionPiperine Enhances the Protective Effect of Curcumin Against 3-NP Induced Neurotoxicity: Possible Neurotransmitters Modulation Mechanism
Singh S, Jamwal S, Kumar P. Piperine Enhances the Protective Effect of Curcumin Against 3-NP Induced Neurotoxicity: Possible Neurotransmitters Modulation Mechanism. Neurochemical Research 2015, 40: 1758-1766. PMID: 26160706, DOI: 10.1007/s11064-015-1658-2.Peer-Reviewed Original ResearchConceptsProtective effectPresence of piperineChronic treatmentMotor deficitsNeuroprotective effectsNeurochemical abnormalitiesAbstract3-Nitropropionic acidPresent studyInduced neurotoxicityMotor functionNeuroprotective activityBody weightMolecular alterationsBeneficial effectsHuntington's diseaseOxidative stressNatural polyphenolNeurotoxicityCurcuminPiperineRatsDiseaseAdministrationBehavioral parametersDaysProtective Effect of Spermidine Against Excitotoxic Neuronal Death Induced by Quinolinic Acid in Rats: Possible Neurotransmitters and Neuroinflammatory Mechanism
Jamwal S, Singh S, Kaur N, Kumar P. Protective Effect of Spermidine Against Excitotoxic Neuronal Death Induced by Quinolinic Acid in Rats: Possible Neurotransmitters and Neuroinflammatory Mechanism. Neurotoxicity Research 2015, 28: 171-184. PMID: 26078029, DOI: 10.1007/s12640-015-9535-y.Peer-Reviewed Original ResearchConceptsQuinolinic acidBody weightQA treatmentGABAergic medium spiny neuronsN-methyl-D-aspartate receptorsOxidative stressGABAergic neuronal lossPro-inflammatory levelsHyperkinetic movement disordersExcitotoxic cell deathAnti-inflammatory propertiesExcitotoxic neuronal deathMedium spiny neuronsReceptor antagonistic propertiesNeuroinflammatory mechanismsPossible neurotransmittersNeuroinflammatory markersNeuronal lossNeuroprotective effectsNeurotransmitter alterationsCatecholamine levelsCascade of eventsNeuronal deathSpiny neuronsMovement disorders
2014
Neuroprotective effect of hemeoxygenase-1/glycogen synthase kinase-3β modulators in 3-nitropropionic acid-induced neurotoxicity in rats
Khan A, Jamwal S, Bijjem K, Prakash A, Kumar P. Neuroprotective effect of hemeoxygenase-1/glycogen synthase kinase-3β modulators in 3-nitropropionic acid-induced neurotoxicity in rats. Neuroscience 2014, 287: 66-77. PMID: 25536048, DOI: 10.1016/j.neuroscience.2014.12.018.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBody WeightCorpus StriatumEncephalitisGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHeme Oxygenase-1HeminLipid PeroxidationLithium ChlorideMaleMetalloporphyrinsMotor ActivityNeuroprotective AgentsNeurotoxicity SyndromesNitritesNitro CompoundsOxidative StressPropionatesProtoporphyrinsRatsRats, WistarRotarod Performance TestSignal TransductionConceptsAdministration of heminHemeoxygenase-1GSK-3β activityN-methyl-D-aspartate receptorsOxidative stressPro-inflammatory mediatorsPresent studyHO-1 inhibitorGSK-3β pathwaySynthase kinase-3β pathwayDifferent neurodegenerative disordersHD-like symptomsProphylactic therapyNeuroprotective effectsPathophysiology of HDTin protoporphyrinMotor impairmentPharmacological modulationMotor coordinationBody weightLocomotor activityMolecular alterationsTherapeutic potentialOxidative burdenNeurodegenerative disorders