Search results for "Neuroprotective Agent"

showing 10 items of 156 documents

Tauroursodeoxycholic acid in the treatment of patients with amyotrophic lateral sclerosis

2015

Background and purpose: Tauroursodeoxycholic acid (TUDCA) is a hydrophilic bile acid that is produced in the liver and used for treatment of chronic cholestatic liver diseases. Experimental studies suggest that TUDCA may have cytoprotective and anti-apoptotic action, with potential neuroprotective activity. A proof of principle approach was adopted to provide preliminary data regarding the efficacy and tolerability of TUDCA in a series of patients with amyotrophic lateral sclerosis (ALS). Methods: As a proof of principle, using a double-blind placebo controlled design, 34 ALS patients under treatment with riluzole who were randomized to placebo or TUDCA (1 g twice daily for 54 weeks) were e…

AdultMale0301 basic medicineamyotrophic lateral sclerosismedicine.medical_specialtyALS - TUDCA - clinical trialmedicine.drug_classPilot ProjectsAmyotrophic lateral sclerosis; Cholic acids; Tauroursodeoxycholic acid; Adult; Aged; Amyotrophic Lateral Sclerosis; Double-Blind Method; Drug Therapy Combination; Female; Humans; Male; Middle Aged; Neuroprotective Agents; Pilot Projects; Riluzole; Taurochenodeoxycholic Acid; Outcome Assessment (Health Care); Neurology; Neurology (clinical)PlaceboNeuroprotectionGastroenterologyTaurochenodeoxycholic AcidOutcome Assessment (Health Care)03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDouble-Blind MethodDrug TherapyInternal medicinemedicineCholic acidHumansAmyotrophic lateral sclerosisAdverse effectAmyotrophic lateral sclerosiAgedtauroursodeoxycholic acidRiluzoleBile acidbusiness.industryTauroursodeoxycholic acidMiddle Agedmedicine.diseaseRiluzoleSurgerySettore MED/26 - NEUROLOGIANeuroprotective Agentscholic acids030104 developmental biologyNeurologychemistryTolerabilityCombinationFemaleNeurology (clinical)business030217 neurology & neurosurgerymedicine.drugEuropean Journal of Neurology
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Analysis of Safety and Tolerability Data Obtained from Over 1,500 Patients Receiving Topiramate for Migraine Prevention in Controlled Trials

2008

Objective.  Topiramate is an effective and generally well-tolerated migraine preventive therapy, as shown in three large, randomized, double-blind, placebo-controlled registration trials. Based upon efficacy/tolerability, topiramate 100 mg/day (50 mg BID) is the recommended target dose for most patients with migraine. To further assess the safety and tolerability of topiramate for migraine prevention, we analyzed safety data from 1,580 patients who participated in the three pivotal registration trials or an earlier pilot, randomized, double-blind, placebo-controlled trial. Methods.  The safety population consisted of all patients who took ≥1 dose of study medication during the double-blind …

AdultTopiramateAdolescentNauseaMigraine DisordersPopulationPhysical examinationFructosePlaceboTopiramatemedicineHumansChildAdverse effecteducationAgedRandomized Controlled Trials as Topiceducation.field_of_studymedicine.diagnostic_testbusiness.industryPatient SelectionDrug ToleranceGeneral MedicineMiddle Agedmedicine.diseaseNeuroprotective AgentsAnesthesiology and Pain MedicineTolerabilityMigraineAnesthesiaNeurology (clinical)Safetymedicine.symptombusinessmedicine.drugPain Medicine
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Neuroprotective effects of behavioural training and nicotine on age-related deficits in spatial learning.

2006

Studies in humans and animals show a clear decline in spatial memory with age and several approaches have been adopted to alleviate this impairment. The purpose of our review is to assess the studies that have suggested the possible neuroprotective actions of behavioural training and nicotine-applied both independently and in conjunction-on age-related deficits in spatial learning. Both spatial pretraining and nonspatial experiences influence an animal's performance in spatial tasks. In aged rats, the experience of training in the water maze task increases the number of newly generated neurons in the hippocampus. The neuroprotective effects of nicotine have been demonstrated in both in-vitr…

AgingNicotineHippocampusWater mazeReceptors NicotinicNeuroprotectionSpatial memoryHippocampusNicotineBehavior TherapyEscape ReactionOrientationmedicineAnimalsHumansMaze LearningProblem SolvingPharmacologyConfoundingNeurodegenerative DiseasesSpatial cognitionRatsPsychiatry and Mental healthNeuroprotective AgentsPractice PsychologicalMental RecallSpatial learningSeptum PellucidumPsychologyCognitive psychologymedicine.drugBehavioural pharmacology
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Pharmacological intervention in age-associated brain disorders by Flupirtine: Alzheimer’s and Prion diseases

1998

Alzheimer's disease, a major form of dementia in the elderly has become an increasingly important health problem in developed countries. In vitro studies on primary neurons demonstrate that Flupirtine (Katadolon) at a concentration of 1 microg/ml, significantly reduces the neurotoxic (apoptotic) effect displayed by A beta25-35, a segment of the amyloid beta-protein precursor the etiologic agent of Alzheimer's disease. Flupirtine, which has been in clinical use since 10 years ago, prevents the toxic effect of PrP, the presumed etiologic agent of the Creutzfeldt-Jakob disease as well as the excitatory amino acid glutamate on cortical neurons. Flupirtine displays a bimodal activity. Its strong…

AgingTime FactorsCell SurvivalPrionsMolecular Sequence DataAminopyridinesApoptosisPharmacologyBiologyNeuroprotectionPrion Diseaseschemistry.chemical_compoundGlutamatesAlzheimer DiseasemedicineAnimalsAmino Acid SequenceRats WistarCells CulturedNeuronsAmyloid beta-PeptidesGlutamate receptorNeurotoxicityBiological activityGlutathionemedicine.diseasePeptide FragmentsRatsNeuroprotective Agentsmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2BiochemistrychemistryCalciumNeuronAlzheimer's diseaseFlupirtineDevelopmental Biologymedicine.drugMechanisms of Ageing and Development
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Fingolimod as a Treatment in Neurologic Disorders Beyond Multiple Sclerosis

2020

Abstract Fingolimod is an approved treatment for relapsing–remitting multiple sclerosis (MS), and its properties in different pathways have raised interest in therapy research for other neurodegenerative diseases. Fingolimod is an agonist of sphingosine-1-phosphate (S1P) receptors. Its main pharmacologic effect is immunomodulation by lymphocyte homing, thereby reducing the numbers of T and B cells in circulation. Because of the ubiquitous expression of S1P receptors, other effects have also been described. Here, we review preclinical experiments evaluating the effects of treatment with fingolimod in neurodegenerative diseases other than MS, such as Alzheimer’s disease or epilepsy. Fingolimo…

AgonistSphingosine 1 Phosphate Receptor ModulatorsMultiple Sclerosismedicine.drug_classDrug Evaluation PreclinicalDiseaseReview ArticleRM1-950PharmacologyNeuroprotection03 medical and health sciencesEpilepsyMice0302 clinical medicineNeurotrophic factorsAlzheimer DiseasemedicineAnimalsHumansLymphocytes030304 developmental biologyPharmacology0303 health sciencesEpilepsyMicrogliabusiness.industryFingolimod HydrochlorideMultiple sclerosisAnti-Inflammatory Agents Non-Steroidalmedicine.diseaseFingolimod3. Good healthRatsDisease Models Animalmedicine.anatomical_structureNeuroprotective AgentsTherapeutics. PharmacologyNervous System Diseasesbusiness030217 neurology & neurosurgerymedicine.drugDrugs in R&D
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Modulatory effects of the novel TrkB receptor agonist 7,8-dihydroxyflavone on synaptic transmission and intrinsic neuronal excitability in mouse visu…

2013

7,8-Dihydroxyflavone (7,8 DHF) is a new recently identified TrkB receptor agonist, which possesses a potent neurotrophic activity and shares many physiological properties with the neurotrophin "Brain Derived Neurotrophic Factor" (BDNF). However, its precise mechanism of action at the cellular level has not been clarified yet. In the present study we explored the effects of this agent on synaptic and intrinsic neuronal properties by performing whole-cell patch clamp recordings from layer 2/3 pyramidal neurons. Incubation of acute cortical slices with 7,8-DHF (20 µM) for 30 min caused a selective reduction in the strength of GABAergic inhibition. The amplitude of evoked inhibitory postsynapti…

Agonistmedicine.drug_classNerve Tissue ProteinsTropomyosin receptor kinase BNeurotransmissionIn Vitro Techniques78-DihydroxyflavoneInhibitory postsynaptic potentialSynaptic TransmissionGlutamatergicMicemedicineElectric ImpedanceAnimalsReceptor trkBGABA-A Receptor AntagonistsGABAergic NeuronsProtein Kinase InhibitorsCells CulturedNootropic AgentsVisual CortexPharmacologyBrain-derived neurotrophic factorbiologyPyramidal CellsNeural InhibitionFlavonesReceptors GABA-AMice Inbred C57BLKineticsNeuroprotective Agentsbiology.proteinEvoked Potentials VisualNeuroscienceNeurotrophinEuropean journal of pharmacology
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Methylprednisolone prevents nerve injury-induced hyperalgesia in neprilysin knockout mice.

2013

The pathophysiology of the complex regional pain syndrome involves enhanced neurogenic inflammation mediated by neuropeptides. Neutral endopeptidase (neprilysin, NEP) is a key enzyme in neuropeptide catabolism. Our previous work revealed that NEP knock out (ko) mice develop more severe hypersensitivity to thermal and mechanical stimuli after chronic constriction injury (CCI) of the sciatic nerve than wild-type (wt) mice. Because treatment with glucocorticoids is effective in early complex regional pain syndrome, we investigated whether methylprednisolone (MP) reduces pain and sciatic nerve neuropeptide content in NEP ko and wt mice with nerve injury. After CCI, NEP ko mice developed more se…

Agonistmedicine.medical_specialtymedicine.drug_classNeuropeptideSubstance PMethylprednisolonechemistry.chemical_compoundMiceInternal medicineMedicineAnimalsNeprilysinMice KnockoutNeurogenic inflammationbusiness.industryfungiNerve injuryMice Inbred C57BLAnesthesiology and Pain MedicineEndocrinologyNeuroprotective AgentsNeurologychemistryHyperalgesiaAnesthesiaHyperalgesiaNeprilysinNeurology (clinical)Sciatic nervemedicine.symptomSciatic NeuropathybusinessPainReferences
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Adaptogens in chemobrain (Part II): Effect of plant extracts on chemotherapy-induced cytotoxicity in neuroglia cells

2019

Abstract Background Cancer chemotherapy-induced cognitive impairments are apparently associated with harmful effects on physiological functions of brain cells. Adaptogens, are known to exhibit neuroprotective effects and to increase cognitive functions in clinical studies. In our previous study (Seo et al., 2018), we demonstrated that selected adaptogenic extracts significantly attenuate cytostatic-induced regulation of more than 100 genes involved in the activation of neuronal death and inhibiting neurogenesis. Neuroprotective and cytoprotective activities of adaptogens rise the question about their possible impact on cytostatic effects of a chemotherapeutic combination of 5-fluorouracil, …

AndrographolidePharmaceutical ScienceEleutherococcusPharmacologyNeuroprotectionCell Linelaw.invention03 medical and health scienceschemistry.chemical_compound0302 clinical medicinelawAntineoplastic Combined Chemotherapy ProtocolsDrug DiscoveryRhodiolamedicineHumansCytotoxic T cellCytotoxicityCyclophosphamideEpirubicin030304 developmental biologyPharmacology0303 health sciencesDose-Response Relationship DrugbiologyPlant ExtractsNeurotoxicitybiology.organism_classificationmedicine.diseaseNeuroprotective AgentsComplementary and alternative medicinechemistry030220 oncology & carcinogenesisMolecular MedicineAndrographisRhodiolaFluorouracilPhytotherapyNeurogliaEpirubicinmedicine.drugPhytomedicine
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Antioxidant Pathways in Alzheimers Disease: Possibilities of Intervention

2011

Alzheimer's disease (AD) is closely related to the occurrence of oxidative stress. It was claimed that all pathophysiological mechanisms involved in the onset and progression of AD are related to oxidative stress. Thus, it is important to evaluate if there is oxidative stress as well as the mechanism by which this happens in AD patients as well as in animal models of AD. Extracellular plaques of amyloid b peptides (Aβ), a hallmark of the disease, have been postulated to be more protective than damaging in terms of oxidative stress because they may be chemical sinks in which heavy metals are placed. More than a decade ago we reasoned that damage due to Ab might be caused not by extracellular…

AntioxidantAmyloidmedicine.medical_treatmentRespiratory chainNerve Tissue ProteinsBiologyPharmacologymedicine.disease_causeAntioxidantsAlzheimer DiseaseDrug DiscoverymedicineExtracellularAnimalsHumansMolecular Targeted TherapyPharmacologychemistry.chemical_classificationReactive oxygen speciesEstradiolVitamin Emedicine.diseaseUp-RegulationOxidative StressNeuroprotective AgentschemistryDietary SupplementsImmunologyAlzheimer's diseaseReactive Oxygen SpeciesOxidative stressCurrent Pharmaceutical Design
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Antioxidant and neuroprotective effects of synthesized sintenin derivatives

2009

Three series of sintenin derivatives (compounds 1-14) were designed and prepared and their antioxidative and neuroprotective effects were evaluated. The in vitro models of scavenging 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals, chelating ferrous ions, inhibiting the rat brain homogenates lipid peroxidation, and protecting neurons damaged by hydrogen peroxide were employed for bioassays. It was found that sintenin derivatives 4 and 13 showed remarkable antioxidative and neuroprotective activities.

AntioxidantDPPHmedicine.medical_treatmentRadicalNeuroprotectionAntioxidantsRats Sprague-DawleyLipid peroxidationchemistry.chemical_compoundPicratesDrug DiscoverymedicineAnimalsChelationHydrogen peroxideCells CulturedChelating AgentsNeuronsPharmacologyChemistryBiphenyl CompoundsHydrogen PeroxideGeneral MedicineRatsBiphenyl compoundNeuroprotective AgentsBiochemistryLipid PeroxidationPropionatesJournal of Enzyme Inhibition and Medicinal Chemistry
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