Search results for "Neuroprotection"

showing 10 items of 326 documents

Atypical 1,4-dihydropyridine derivatives, an approach to neuroprotection and memory enhancement

2016

This mini review is devoted to the design and pharmacological studies of novel atypical 1,4-dihydropyridine (DHP) derivatives which differ to a great extent from the traditional DHPs either by lack of neuronal calcium channel blocking activity and/or inability to protect mitochondrial processes. About 100 new DHP derivatives were screened and the mostly active were selected for detailed studies. The compounds of the series of the amino acid ("free" plus "crypto")-containing DHPs and lipophilic di-cyclic DHPs demonstrated long-lasting neuroprotective and/or memory-enhancing action, particularly at low doses (0.005-0.05mg/kg) in different neurodeficiency rat or mice models, and exerted neurot…

0301 basic medicineGenetically modified mouseDihydropyridinesDHPSNeurotransmissionBiologyPharmacologyNeuroprotection03 medical and health sciences0302 clinical medicineMemoryAnimalsHumansPharmacologychemistry.chemical_classificationNeurotransmitter AgentsCalcium channelCalcium Channel BlockersNeuroprotectionAmino acid030104 developmental biologychemistrySynaptic plasticityNervous System DiseasesNeurotransmitter AgentsNeuroscience030217 neurology & neurosurgeryPharmacological Research
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Autoimmune aspects in glaucoma

2016

The pathogenesis of glaucoma, a common neurodegenerative disease, involves an immunologic component. Studies demonstrate changes of autoantibody concentrations against retinal and optic nerve head antigens in glaucoma patients. Furthermore we found antibody deposits in human glaucomatous retinae in a pro-inflammatory environment. Clinical studies showed up regulated, but also significantly down-regulated autoantibody levels. These antibodies belong to the natural autoimmunity. The upregulation of autoantibodies can be associated with fatal conditions, but several studies demonstrate that natural autoantibodies entail also neuroprotective characteristics and influence the protein expression …

0301 basic medicineGlaucomaAutoimmunityDiseasemedicine.disease_causeNeuroprotectionAutoimmunityPathogenesis03 medical and health sciences0302 clinical medicineAntigenmedicineAnimalsHumansAutoantibodiesPharmacologybusiness.industryAutoantibodyGlaucomamedicine.diseaseNeuroprotection030104 developmental biologyImmunology030221 ophthalmology & optometryBiomarker (medicine)sense organsbusinessEuropean Journal of Pharmacology
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Neuroprotective and Anti-Inflammatory Effects of a Hydrophilic Saffron Extract in a Model of Glaucoma

2019

Glaucoma is a neurodegenerative disease characterized by the loss of retinal ganglion cells (RGCs). An increase in the intraocular pressure is the principal risk factor for such loss, but controlling this pressure does not always prevent glaucomatous damage. Activation of immune cells resident in the retina (microglia) may contribute to RGC death. Thus, a substance with anti-inflammatory activity may protect against RGC degeneration. This study investigated the neuroprotective and anti-inflammatory effects of a hydrophilic saffron extract standardized to 3% crocin content in a mouse model of unilateral, laser-induced ocular hypertension (OHT). Treatment with saffron extract decreased microg…

0301 basic medicineIntraocular pressureretinagenetic structuresAnti-Inflammatory AgentsOcular hypertensionmicrogliaPharmacologysaffron extractneuroinflammationCrocinlcsh:ChemistryMicechemistry.chemical_compound0302 clinical medicinelcsh:QH301-705.5SpectroscopyIba-1General MedicineComputer Science ApplicationsNeuroprotective Agentsmedicine.anatomical_structureRetinal ganglion cellOftalmologíaneuroprotectionHydrophobic and Hydrophilic InteractionsNeurocienciasRetinal ganglionNeuroprotectionArticleCatalysisganglion cellsInorganic Chemistry03 medical and health sciencesP2RY12medicineAnimalsPhysical and Theoretical ChemistryMolecular BiologyIntraocular PressureNeuroinflammationexperimental glaucomaRetinaPlant Extractsbusiness.industryOrganic ChemistryBrn3aGlaucomaCrocusmedicine.diseaseAnatomía oculareye diseasesDisease Models Animal030104 developmental biologychemistrylcsh:Biology (General)lcsh:QD1-999sense organsbusinessBiomarkers030217 neurology & neurosurgeryInternational Journal of Molecular Sciences
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In vivo and in vitro effects of multiple sclerosis immunomodulatory therapeutics on glutamatergic excitotoxicity.

2015

In multiple sclerosis (MS), a candidate downstream mechanism for neuronal injury is glutamate (Glu)-induced excitotoxicity, leading to toxic increases in intraneuronal Ca(2+) . Here, we used in vivo two-photon imaging in the brain of TN-XXL transgenic Ca(2+) reporter mice to test whether promising oral MS therapeutics, namely fingolimod, dimethyl fumarate, and their respective metabolites fingolimod-phosphate and monomethyl fumarate, can protect neurons against acute glutamatergic excitotoxic damage. We also assessed whether these drugs can protect against excitotoxicity in vitro using primary cortical neurons, and whether they can directly inhibit Glu release from pathogenic T-helper 17 ly…

0301 basic medicineKainic acidMultiple SclerosisExcitotoxicityGlutamic AcidPharmacologyBiologymedicine.disease_causeBiochemistryNeuroprotectionImmunomodulation03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineIn vivomedicineAnimalsCells CulturedNeuronsKainic AcidDimethyl fumarateCell DeathGlutamate receptorNeurotoxicityBrainmedicine.diseaseUp-Regulation030104 developmental biologyNeuroprotective AgentschemistryNMDA receptor030217 neurology & neurosurgerySignal TransductionJournal of neurochemistry
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Medicinal Plants and Natural Products as Potential Sources for Antiparkinson Drugs

2016

Parkinsonʼs disease is a progressive neurodegenerative dysfunction characterized by the loss of pigmented dopaminergic neurons of the nigrostriatal system with a consequent dopamine decrease. The reduction of dopamine levels produces neuronal damage, depigmentation of the substantia nigra, and the presence of intracellular inclusions in dopaminergic neurons. Treatments for Parkinsonʼs disease aim for improving these motor symptoms by increasing the dopaminergic signal in the striatum with levodopa in combination with enzyme inhibitors or anticholinergic drugs. Nevertheless, natural products can act as neuroprotective agents by reducing the progression of the disease and the inflammatory pro…

0301 basic medicineLevodopaPharmaceutical ScienceSubstantia nigraPharmacologyBiologyNeuroprotectionAnalytical ChemistryAntiparkinson Agents03 medical and health sciences0302 clinical medicineDopamineDrug DiscoverymedicineAnimalsHumansPharmacologyBiological ProductsPlants MedicinalPlant ExtractsOrganic ChemistryDopaminergicAntiparkinsonian AgentAntiparkinson drug030104 developmental biologynervous systemComplementary and alternative medicineAntiparkinson AgentsMolecular Medicine030217 neurology & neurosurgeryPhytotherapymedicine.drugPlanta Medica
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Molecular mechanisms underlying the neuroprotective role of atrial natriuretic peptide in experimental acute ischemic stroke

2018

Abstract Along with its role in regulating blood pressure and fluid homeostasis, the natriuretic peptide system could be also part of an endogenous protective mechanism against brain damage. We aimed to assess the possibility that exogenous atrial natriuretic peptide (ANP) could protect against acute ischemic stroke, as well as the molecular mechanisms involved. Three groups of rats subjected to transient middle cerebral artery occlusion (tMCAO, intraluminal filament technique, 60 min) received intracerebroventricular vehicle, low-dose ANP (0.5 nmol) or high-dose ANP (2.5 nmol), at 30 min reperfusion. Neurofunctional condition, and brain infarct and edema volumes were measured at 24 h after…

0301 basic medicineMAPK/ERK pathwayMalePotassium ChannelsSignaling pathwaysmedicine.drug_classMAP Kinase Signaling SystemAcute ischemic strokeDown-RegulationApoptosisBrain damagePharmacologyBiochemistryNeuroprotectionBrain Ischemia03 medical and health sciencesPhosphatidylinositol 3-Kinases0302 clinical medicineEndocrinologyAtrial natriuretic peptideNatriuretic peptideMedicineAnimalsDNA CleavageRats WistarReceptorAtrial natriuretic peptideMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayInjections Intraventricularbusiness.industryCaspase 3Natriuretic peptide receptorsBrainInfarction Middle Cerebral ArteryStroke030104 developmental biologyNeuroprotective AgentsReperfusion InjuryK+ channelsmedicine.symptombusinessProto-Oncogene Proteins c-aktReceptors Atrial Natriuretic Factor030217 neurology & neurosurgeryAtrial Natriuretic Factorhormones hormone substitutes and hormone antagonists
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Resting-state posterior alpha rhythms are abnormal in subjective memory complaint seniors with preclinical Alzheimer's neuropathology and high educat…

2020

International audience; Cognitive reserve is present in Alzheimer's disease (AD) seniors with high education attainment making them clinically resilient to extended brain neuropathology and neurodegeneration. Here, we tested whether subjective memory complaint (SMC) seniors with AD neuropathology and high education attainment of the prospective INSIGHT-preAD cohort (Paris) may present abnormal eyesclosed resting state posterior electroencephalographic rhythms around individual alpha frequency peak, typically altered in AD patients. The SMC participants negative to amyloid PET AD markers (SMCneg) with high (over low-moderate) education level showed higher posterior alpha 2 power density (pos…

0301 basic medicineMaleAgingpsychology [Alzheimer Disease]alpha rhythms; INSIGHT-preAD study; preclinical Alzheimer's disease (AD); preclinical Alzheimer's neuropathology; resting state EEG rhythms; subjective memory complaint (SMC)physiopathology [Brain]Cohort Studies0302 clinical medicineCognitive ReserveMedicineProspective StudiesCognitive reserveAged 80 and over[SDV.NEU.PC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Psychology and behavior4. EducationGeneral NeuroscienceNeurodegenerationdiagnosis [Alzheimer Disease]BrainCognitionElectroencephalographyMagnetic Resonance ImagingAlpha Rhythm[SCCO.PSYC]Cognitive science/PsychologyEducational StatusFemale[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]RestAlpha (ethology)NeuropathologyNeuroprotectionphysiopathology [Alzheimer Disease]03 medical and health sciencesRhythmAlzheimer DiseaseMemoryHumansddc:610AgedResting state fMRIbusiness.industry[SCCO.NEUR]Cognitive science/Neurosciencemedicine.disease030104 developmental biologyphysiology [Rest]Positron-Emission TomographyNeurology (clinical)Geriatrics and GerontologybusinessNeuroscience030217 neurology & neurosurgeryDevelopmental Biology
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Very low doses of muscimol and baclofen ameliorate cognitive deficits and regulate protein expression in the brain of a rat model of streptozocin-ind…

2018

Recent studies devoted to neuroprotection have focused on the role of the gamma-aminobutyric acid (GABA) system in regulating neuroinflammatory processes which play a key role in the neurodegenerative processes observed in Alzheimer's disease (AD) by inducing glial cell overactivation and impairing neurotransmission. Data on the efficacy of classical GABA-A and GABA-B receptor agonists (muscimol and baclofen, respectively) in animal models of AD are not available. Moreover, no published studies have examined the ability of optimal doses of these compounds to prevent neuroinflammation, the alterations in neurotransmission and cognitive deficits. In the present study, we used a non-transgenic…

0301 basic medicineMaleBaclofenGlutamate decarboxylaseSpatial LearningPharmacologyNeuroprotectionStreptozocin03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCognitionGABA receptorSTZAlzheimer DiseaseMemoryGlial Fibrillary Acidic ProteinLearningAnimalsRats WistarNeuroinflammationPharmacologyGlial fibrillary acidic proteinbiologyDose-Response Relationship DrugChemistryGABAA receptorMuscimolBrainRatsDisease Models Animal030104 developmental biologyBaclofennervous systemMuscimolGene Expression RegulationRat model of ADbiology.protein:MEDICINE::Physiology and pharmacology::Pharmacological research [Research Subject Categories]Neuroscience030217 neurology & neurosurgeryEuropean journal of pharmacology
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Dimethyl fumarate treatment after traumatic brain injury prevents depletion of antioxidative brain glutathione and confers neuroprotection.

2017

Dimethyl fumarate (DMF) is an immunomodulatory compound to treat multiple sclerosis and psoriasis with neuroprotective potential. Its mechanism of action involves activation of the antioxidant pathway regulator Nuclear factor erythroid 2-related factor 2 thereby increasing synthesis of the cellular antioxidant glutathione (GSH). The objective of this study was to investigate whether post-traumatic DMF treatment is beneficial after experimental traumatic brain injury (TBI). Adult C57Bl/6 mice were subjected to controlled cortical impact followed by oral administration of DMF (80 mg/kg body weight) or vehicle at 3, 24, 48, and 72 h after the inflicted TBI. At 4 days after lesion (dal), DMF-tr…

0301 basic medicineMaleTraumatic brain injuryDimethyl FumarateBrain damagePharmacologyBlood–brain barrierBiochemistryNeuroprotectionAntioxidantsLesion03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineBrain Injuries TraumaticmedicineAnimalsNeuroinflammationDimethyl fumarateGlutathionemedicine.diseaseGlutathioneNeuroprotectionMice Inbred C57BLDisease Models AnimalOxidative Stress030104 developmental biologymedicine.anatomical_structureNeuroprotective AgentsBiochemistrychemistryBlood-Brain Barriermedicine.symptom030217 neurology & neurosurgeryJournal of neurochemistry
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Uric acid treatment after stroke modulates the Krüppel-like factor 2-VEGF-A axis to protect brain endothelial cell functions: Impact of hypertension

2019

Uric acid (UA) is a promising protective treatment in ischaemic stroke, but the precise molecular targets underlying its in vivo beneficial actions remain unclear. High concentrations of UA inhibit angiogenesis of cultured endothelial cells via Krüppel-like factor 2 (KLF)-induced downregulation of vascular endothelial growth factor (VEGF), a pro-angiogenic mediator that is able to increase blood–brain barrier (BBB) permeability in acute stroke. Here, we investigated whether UA treatment after ischaemic stroke protects brain endothelial cell functions and modulates the KLF2-VEGF-A axis. Transient intraluminal middle cerebral artery (MCA) occlusion/reperfusion was induced in adult male sponta…

0301 basic medicineMaleVascular Endothelial Growth Factor AVascular endothelial growth factor-AAngiogenesisBiochemistryRats Inbred WKYAntioxidantschemistry.chemical_compound0302 clinical medicineRats Inbred SHRIschaemic strokeEvans BlueBlood-brain barrierBrainKrüppel-like factor 2Vascular endothelial growth factorEndothelial stem cellStrokeVascular endothelial growth factor Amedicine.anatomical_structureNeuroprotective AgentsTreatment OutcomeBlood-Brain Barrier030220 oncology & carcinogenesisHypertensioncardiovascular systemmedicine.symptommedicine.medical_specialtyKruppel-Like Transcription FactorsBrain damageBlood–brain barrierNeuroprotectionCell Line03 medical and health sciencesDouble-Blind MethodInternal medicinemedicineAnimalsHumanscardiovascular diseasesPharmacologybusiness.industryRatsUric Acid030104 developmental biologyEndocrinologychemistryEndothelium VascularAngiogenesisbusinessBiomarkers
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