Search results for "Neuroprotection"

showing 10 items of 326 documents

Neuroprotective potential of antihyperglycemic drug metformin in streptozocin-induced rat model of sporadic Alzheimer's disease.

2020

Abstract The earliest hallmarks of sporadic Alzheimer's disease (sAD) are impaired glucose metabolism, chronic neuroinflammation, diminished synaptic plasticity and subsequent cognitive decline. The safest antidiabetic drug metformin has shown both glucose metabolism-improving and cognition-enhancing action in type 2 diabetes patients and diabetic model animals. However, metformin has not been previously studied in intracerebroventricular streptozocin (STZ)-induced model of sAD. Therefore, our aim was to assess the preventive action of metformin in sAD model-rats. Firstly, the actions of metformin (75 and 100 mg/kg) on cognitive functions and sociability were examined. Secondly, we wanted t…

0301 basic medicineMaleendocrine system diseasesNerve Tissue ProteinsType 2 diabetesPharmacologyGPI-Linked ProteinsNeuroprotectionStreptozocin03 medical and health sciencesGlycogen Synthase Kinase 30302 clinical medicineCognitionAlzheimer DiseaseMorris Water Maze TestMedicineAnimalsHypoglycemic AgentsCognitive declineRats WistarSocial BehaviorNeuroinflammationInjections IntraventricularPharmacologyGlucose Transporter Type 1Behavior AnimalGlucose Transporter Type 3business.industrydigestive oral and skin physiologyGlucose transporternutritional and metabolic diseasesBrainmedicine.diseaseMetforminMetforminAstrogliosisDisease Models Animal030104 developmental biologyGlucoseNeuroprotective AgentsSynaptic plasticityAcetylcholinesterasebusinessNeuroglia030217 neurology & neurosurgerymedicine.drugEuropean journal of pharmacology
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GABA-containing compound gammapyrone protects against brain impairments in Alzheimer's disease model male rats and prevents mitochondrial dysfunction…

2018

Neuroinflammation, oxidative stress, decreased glucose/energy metabolism, and disrupted neurotransmission are changes that occur early in sporadic Alzheimer's disease (AD), manifesting as mild cognitive impairment. Recently, the imbalanced function of the gamma-aminobutyric acid (GABA) system was identified as a critical factor in AD progression. Thus, maintaining balance among neurotransmitter systems, particularly the GABA system, can be considered a beneficial strategy to slow AD progression. The present study investigated the effects of the compound gammapyrone, a molecule containing three GABA moieties: "free" moiety attached to the position 4 of the 1,4-dihydropyridine (DHP) ring, and…

0301 basic medicineMalemedicine.medical_specialtyAllosteric regulationbioenergetics; GABA; intracerebroventricular streptozocin; PC12 cells; protein expression; spatial learning/memoryNeurotransmissionspatial learning/memorymedicine.disease_causebioenergeticsNeuroprotection03 medical and health sciencesCellular and Molecular NeuroscienceGABA0302 clinical medicineReceptors GABAAlzheimer DiseaseMemoryInternal medicinemedicineAnimalsRats WistarReceptorMaze Learningprotein expressionNeuroinflammationCells Culturedgamma-Aminobutyric AcidGABAA receptorChemistryGlutamate DecarboxylasePC12 cellsBrainintracerebroventricular streptozocinMitochondriaStreptozocinDisease Models Animal030104 developmental biologyEndocrinologyNeuroprotective AgentsAstrocytesAcetylcholinesteraseEncephalitisMicroglia030217 neurology & neurosurgeryOxidative stressJournal of neuroscience research
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Glucagon-like peptide-2 reduces the obesity-associated inflammation in the brain.

2018

Growing evidence suggests a link between obesity and neurodegeneration. The purpose of the present study was to explore the neuroprotective potential of glucagon-like peptide-2 (GLP-2) in the brain of high fat diet (HFD)-fed mice. Markers of inflammation and oxidative stress were analysed in the brains of obese mice chronically treated with [Gly2]-GLP-2 (teduglutide), the stable analogue of the GLP-2, and they were compared to age-matched untreated obese and lean animals. Neurodegeneration was examined by TUNEL assay. HFD feeding increased the expression of pro-inflammatory mediators (NF-kB, IL-8, TNF-α, IL-1β and IL-6), glial fibrillary acidic protein (GFAP), index of gliosis and neurodege…

0301 basic medicineMalemedicine.medical_specialtyInflammationmedicine.disease_causeDiet High-FatSettore BIO/09 - FisiologiaNeuroprotectionlcsh:RC321-57103 medical and health sciences0302 clinical medicineNeuroinflammationInternal medicinemedicineGlucagon-Like Peptide 2AnimalsObesityNeurodegenerationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryNeuroinflammationTUNEL assayGlial fibrillary acidic proteinbiologyChemistryNeurodegenerationdigestive oral and skin physiologyBrainmedicine.diseaseMice Inbred C57BL030104 developmental biologyEndocrinologyNeuroprotective AgentsNeurologyGliosisOxidative stressAstrocytesbiology.proteinGlucagon-Like Peptide-2 ReceptorOxidative streEncephalitismedicine.symptomInflammation MediatorsGLP-2030217 neurology & neurosurgeryOxidative stresshormones hormone substitutes and hormone antagonistsNeurobiology of disease
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Emergent Uric Acid Treatment is Synergistic with Mechanical Recanalization in Improving Stroke Outcomes in Male and Female Rats.

2018

Preclinical and clinical studies support a promising, albeit not definitive, neuroprotective effect of emergent uric acid (UA) administration in ischemic stroke. We assessed the effects of UA in an ischemic stroke model relevant to the current treatment paradigm of mechanical thrombectomy within the STAIR/RIGOR recommendations. A cohort of male and female Wistar rats was subjected to ischemic stroke with mechanical recanalization under physiological monitoring. The effects of transient middle cerebral artery occlusion (tMCAO) with adjunctive UA (IV, 16 mg/kg) or vehicle treatment were assessed at 24 h and 7 days. Outcomes included neurofunctional impairment, brain infarct (TTC staining, MRI…

0301 basic medicineMalemedicine.medical_specialtyMechanical ThrombolysisBrain damageNeuroprotectionBrain Ischemia03 medical and health sciencesCresyl violetchemistry.chemical_compoundRandom Allocation0302 clinical medicineuric acidInternal medicineEdemamedicineischemic strokeAnimalsRats WistarStrokebusiness.industryGeneral Neurosciencerat modeladjunctive treatmentBrainRecovery of Functionmedicine.diseaseCombined Modality TherapyUric AcidStrokeDisease Models Animal030104 developmental biologyNeuroprotective AgentschemistrythrombectomyAdjunctive treatmentIschemic strokeCardiologyUric acidneuroprotectionFemalemedicine.symptombusiness030217 neurology & neurosurgeryNeuroscience
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Sex hormones modulate pathogenic processes in experimental traumatic brain injury.

2018

Clinical and animal studies have revealed sex-specific differences in histopathological and neurological outcome after traumatic brain injury (TBI). The impact of perioperative administration of sex steroid inhibitors on TBI is still elusive. Here, we subjected male and female C57Bl/6N mice to the controlled cortical impact (CCI) model of TBI and applied pharmacological inhibitors of steroid hormone synthesis, that is, letrozole (LET, inhibiting estradiol synthesis by aromatase) and finasteride (FIN, inhibiting dihydrotestosterone synthesis by 5α-reductase), respectively, starting 72 h prior CCI, and continuing for a further 48 h after CCI. Initial gene expression analyses showed that andro…

0301 basic medicineMalemedicine.medical_specialtyanimal structuresmedicine.drug_classmedicine.medical_treatmentTropomyosin receptor kinase BTropomyosin receptor kinase ABiochemistryNeuroprotection03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineInternal medicineBrain Injuries TraumaticmedicineAnimalsNerve Growth FactorsSex CharacteristicsbiologyEstradiolbusiness.industryEstrogen AntagonistsBrainDihydrotestosteroneAndrogennervous system diseasesMice Inbred C57BLSteroid hormoneDisease Models Animal030104 developmental biologyEndocrinologynervous systemSex steroidDihydrotestosteronebiology.proteinFemalebusiness030217 neurology & neurosurgeryNeurotrophinmedicine.drugJournal of neurochemistry
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The Role of NF-κB Triggered Inflammation in Cerebral Ischemia

2021

Cerebral ischemia is a devastating disease that affects many people worldwide every year. The neurodegenerative damage as a consequence of oxygen and energy deprivation, to date, has no known effective treatment. The ischemic insult is followed by an inflammatory response that involves a complex interaction between inflammatory cells and molecules which play a role in the progression towards cell death. However, there is presently a matter of controversy over whether inflammation could either be involved in brain damage or be a necessary part of brain repair. The inflammatory response is triggered by inflammasomes, key multiprotein complexes that promote secretion of pro-inflammatory cytoki…

0301 basic medicineMini ReviewIschemiaNeurosciences. Biological psychiatry. NeuropsychiatryContext (language use)InflammationBrain damageCervell Ferides i lesionsNeuroprotectionNF-κBcerebral ischemia03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicinemedicinebusiness.industryNeurodegenerationneurodegenerationNF-κBInflammasomemedicine.disease030104 developmental biologychemistryinflammationCellular Neuroscienceneuroprotectionmedicine.symptombusinessOxigen Efectes fisiològicsNeuroscience030217 neurology & neurosurgeryRC321-571medicine.drugFrontiers in Cellular Neuroscience
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Neurodegenerative diseases: Might citrus flavonoids play a protective role?

2016

Neurodegenerative diseases (ND) result from the gradual and progressive degeneration of the structure and function of the central nervous system or the peripheral nervous system or both. They are characterized by deterioration of neurons and/or myelin sheath, disruption of sensory information transmission and loss of movement control. There is no effective treatment for ND, and the drugs currently marketed are symptom-oriented, albeit with several side effects. Within the past decades, several natural remedies have gained attention as potential neuroprotective drugs. Moreover, an increasing number of studies have suggested that dietary intake of vegetables and fruits can prevent or delay th…

0301 basic medicineNervous systemCitrusCitruPharmaceutical ScienceReviewDegeneration (medical)Analytical Chemistry0302 clinical medicineDrug DiscoveryNeuropharmacologyTraditional medicineNeurodegenerationfood and beveragesNeurodegenerative Diseases3. Good healthNeuroprotective Agentsmedicine.anatomical_structureChemistry (miscellaneous)Myelin sheathMolecular MedicineNutraceuticalHumanCitrus; Flavonoids; Neurodegeneration; Neurodegenerative disorders; Nutraceutical; Citrus; Fruit; Humans; Neurodegenerative Diseases; Flavonoids; Neuroprotective Agents; Organic ChemistryNeuroprotective AgentBiologyNeuroprotectionlcsh:QD241-44103 medical and health sciencesNutraceuticallcsh:Organic chemistrySettore MED/43 - Medicina LegalemedicineHumansEffective treatmentPhysical and Theoretical ChemistryNeurodegenerationFlavonoidsNeurodegenerative Diseasebusiness.industryOrganic ChemistryCitrus; Flavonoids; Neurodegeneration; Neurodegenerative disorders; Nutraceutical; Medicine (all);Neurodegenerative disordermedicine.diseaseBiotechnology030104 developmental biologyFruitNeurodegenerative disordersFlavonoidSettore BIO/14 - Farmacologiabusiness030217 neurology & neurosurgery
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Lactate as a Metabolite and a Regulator in the Central Nervous System

2016

More than two hundred years after its discovery, lactate still remains an intriguing molecule. Considered for a long time as a waste product of metabolism and the culprit behind muscular fatigue, it was then recognized as an important fuel for many cells. In particular, in the nervous system, it has been proposed that lactate, released by astrocytes in response to neuronal activation, is taken up by neurons, oxidized to pyruvate and used for synthesizing acetyl-CoA to be used for the tricarboxylic acid cycle. More recently, in addition to this metabolic role, the discovery of a specific receptor prompted a reconsideration of its role, and lactate is now seen as a sort of hormone, even invol…

0301 basic medicineNervous systemlactate transporterCentral nervous systemReviewBiologyBlood–brain barrierlactate receptorsNeuroprotectionCatalysislcsh:ChemistryInorganic Chemistry03 medical and health sciences0302 clinical medicineSettore BIO/10 - Biochimicalactate receptormedicineAnimalsHumanslactate transportersPhysical and Theoretical ChemistryReceptorExerciselcsh:QH301-705.5Molecular BiologySpectroscopyOrganic ChemistryNeurodegenerationlactic acidBrainGeneral MedicineMetabolismblood-brain barriermedicine.diseaseComputer Science ApplicationsCitric acid cycle030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)lcsh:QD1-999Biochemistrybrain metabolismActic acidexercise and lactateEnergy MetabolismNeuroscience030217 neurology & neurosurgerySignal Transductionactic acid; brain metabolism; lactate transporters; blood-brain barrier; lactate receptors; exercise and lactate
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Protein misfolding, amyotrophic lateral sclerosis and guanabenz: Protocol for a phase II RCT with futility design (ProMISe trial)

2017

IntroductionRecent studies suggest that endoplasmic reticulum stress may play a critical role in the pathogenesis of amyotrophic lateral sclerosis (ALS) through an altered regulation of the proteostasis, the cellular pathway-balancing protein synthesis and degradation. A key mechanism is thought to be the dephosphorylation of eIF2α, a factor involved in the initiation of protein translation. Guanabenz is an alpha-2-adrenergic receptor agonist safely used in past to treat mild hypertension and is now an orphan drug. A pharmacological action recently discovered is its ability to modulate the synthesis of proteins by the activation of translational factors preventing misfolded protein accumula…

0301 basic medicineOncologyPathologyamyotrophic lateral sclerosisamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response; adrenergic alpha-2 receptor agonist s; age of onset; amyotrophic lateral sclerosis; disease progression; double-blind method; endoplasmic reticulum stress; guanabenz; humans; italy; medical futility; neuroprotective agents; proteostasis deficienciesamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response; Medicine (all)randomized clinical trial guanabenzHelsinki declaration0302 clinical medicineProtocolAdrenergic alpha-2 Receptor Agonists1506Amyotrophic lateral sclerosisAge of OnsetGuanabenzMedicine (all)amyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein responseNeurodegenerationamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response;amyotrophic lateral sclerosis; guanabenz; motor neurone disease; neuromuscular disease; randomized clinical trial; unfolded protein response; Adrenergic alpha-2 Receptor Agonists; Age of Onset; Amyotrophic Lateral Sclerosis; Disease Progression; Double-Blind Method; Endoplasmic Reticulum Stress; Guanabenz; Humans; Italy; Medical Futility; Neuroprotective Agents; Proteostasis DeficienciesGeneral Medicineunfolded protein responseEndoplasmic Reticulum StressRiluzoleNeuroprotective AgentsNeurologyTolerabilityItalyDisease Progression1713GuanabenzMedical Futilitymedicine.drugmedicine.medical_specialtyamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response; Adrenergic alpha-2 Receptor Agonists; Age of Onset; Amyotrophic Lateral Sclerosis; Disease Progression; Double-Blind Method; Endoplasmic Reticulum Stress; Guanabenz; Humans; Italy; Medical Futility; Neuroprotective Agents; Proteostasis Deficiencies; Medicine (all)Neuroprotection03 medical and health sciencesmotor neurone diseaseDouble-Blind MethodInternal medicinemedicineHumansProteostasis Deficienciesbusiness.industryAmbientaleneuromuscular diseaserandomized clinical trialmedicine.diseaseClinical trial030104 developmental biologybusiness030217 neurology & neurosurgery
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An update on intracerebral stem cell grafts.

2018

Introduction: Primary neurological disorders are notoriously debilitating and deadly, and over the past four decades stem cell therapy has emerged as a promising treatment. Translation of stem cell therapies from the bench to the clinic requires a better understanding of delivery protocols, safety profile, and efficacy in each disease. Areas covered: In this review, benefits and risks of intracerebral stem cell transplantation are presented for consideration. Milestone discoveries in stem cell applications are reviewed to examine the efficacy and safety of intracerebral stem cell transplant therapy for disorders of the central nervous system and inform design of translatable protocols for c…

0301 basic medicineOncologymedicine.medical_specialtyParkinson's diseaseTraumatic brain injurymedicine.medical_treatmentmulti-system atrophyNeuroprotection03 medical and health sciencesGraft vs Host Reaction0302 clinical medicineHuntington's diseaseCentral Nervous System DiseasesRisk FactorsInternal medicineMedicineAnimalsHumansPharmacology (medical)amyotrophic lateral sclerosiAmyotrophic lateral sclerosisStem cellbusiness.industryGeneral NeuroscienceMultiple sclerosistraumatic brain injuryStem-cell therapymedicine.diseasestroke030104 developmental biologyBlood-Brain Barriermultiple sclerosiParkinson’s diseaseneuroprotectionNeurology (clinical)Stem cellbusiness030217 neurology & neurosurgeryHuntington’s diseaseStem Cell TransplantationExpert review of neurotherapeutics
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