Search results for "Brain"

showing 10 items of 3997 documents

Forager age and foraging state, but not cumulative foraging activity, affect biogenic amine receptor gene expression in the honeybee mushroom bodies

2020

Foraging behavior is crucial for the development of a honeybee colony. Biogenic amines are key mediators of learning and the transition from in-hive tasks to foraging. Foragers vary considerably in their behavior, but whether and how this behavioral diversity depends on biogenic amines is not yet well understood. For example, forager age, cumulative foraging activity or foraging state may all be linked to biogenic amine signaling. Furthermore, expression levels may fluctuate depending on daytime. We tested if these intrinsic and extrinsic factors are linked to biogenic amine signaling by quantifying the expression of octopamine, dopamine and tyramine receptor genes in the mushroom bodies, i…

0301 basic medicineForagingGene ExpressionZoologyBiologyAffect (psychology)03 medical and health sciencesBehavioral Neuroscience0302 clinical medicineReceptors Biogenic AmineBiogenic amineGene expressionGeneticsAnimalsLearningReceptorMushroom Bodieschemistry.chemical_classificationBehavior AnimalAge FactorsBrainFeeding BehaviorBeesBiogenic amine receptor030104 developmental biologyNeurologychemistryMushroom bodiesOctopamine (neurotransmitter)030217 neurology & neurosurgeryGenes, Brain and Behavior
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Crosstalk between receptor tyrosine kinases (RTKs) and G protein-coupled receptors (GPCR) in the brain: Focus on heteroreceptor complexes and related…

2019

Neuronal events are regulated by the integration of several complex signaling networks in which G protein-coupled receptors (GPCRs) and receptor tyrosine kinases (RTKs) are considered key players of an intense bidirectional cross-communication in the cell, generating signaling mechanisms that, at the same time, connect and diversify the traditional signal transduction pathways activated by the single receptor. For this receptor-receptor crosstalk, the two classes of receptors form heteroreceptor complexes resulting in RTKs transactivation and in growth-promoting signals. In this review, we describe heteroreceptor complexes between GPCR and RTKs in the central nervous system (CNS) and their …

0301 basic medicineG proteinRTKHeteroreceptorSettore BIO/09 - FisiologiaReceptor tyrosine kinaseReceptors G-Protein-Coupled03 medical and health sciencesCellular and Molecular NeuroscienceTransactivation0302 clinical medicineGPCRReceptor Fibroblast Growth Factor Type 1Receptor Fibroblast Growth Factor Type 2ReceptorG protein-coupled receptorPharmacologyTransactivationbiologyChemistryReceptor Protein-Tyrosine KinasesBrainReceptor Cross-TalkCrosstalk (biology)030104 developmental biologyHeteroreceptor complexebiology.proteinSignal transductionNeuroscience030217 neurology & neurosurgerySignal Transduction
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ESC-Derived BDNF-Overexpressing Neural Progenitors Differentially Promote Recovery in Huntington's Disease Models by Enhanced Striatal Differentiation

2016

Summary Huntington's disease (HD) is characterized by fatal motoric failures induced by loss of striatal medium spiny neurons. Neuronal cell death has been linked to impaired expression and axonal transport of the neurotrophin BDNF (brain-derived neurotrophic factor). By transplanting embryonic stem cell-derived neural progenitors overexpressing BDNF, we combined cell replacement and BDNF supply as a potential HD therapy approach. Transplantation of purified neural progenitors was analyzed in a quinolinic acid (QA) chemical and two genetic HD mouse models (R6/2 and N171-82Q) on the basis of distinct behavioral parameters, including CatWalk gait analysis. Explicit rescue of motor function by…

0301 basic medicineGene ExpressionBiochemistrychemistry.chemical_compoundMice0302 clinical medicineNeural Stem CellsNeurotrophic factorsGenes Reporterlcsh:QH301-705.5Neuronslcsh:R5-920NeurogenesisCell DifferentiationAnatomyembryonic stem cellsHuntington Diseaselcsh:Medicine (General)NeurogliaLocomotionNeurotrophinHuntington’s diseaseCell SurvivalBiologyMedium spiny neuronArticle03 medical and health sciencesHuntington's diseaseGeneticsmedicinestriatal differentiationAnimalsBrain-derived neurotrophic factorBrain-Derived Neurotrophic FactorCell Biologymedicine.diseaseCorpus StriatumTransplantationDisease Models Animal030104 developmental biologylcsh:Biology (General)chemistrynervous systembiology.proteinNeuroscience030217 neurology & neurosurgeryBiomarkersDevelopmental BiologyQuinolinic acidStem Cell TransplantationStem Cell Reports
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MiR-144 overexpression as a promising therapeutic strategy to overcome glioblastoma cell invasiveness and resistance to chemotherapy

2019

Abstract Glioblastoma (GB) is the most aggressive and common form of primary brain tumor, characterized by fast proliferation, high invasion, and resistance to current standard treatment. The average survival rate post-diagnosis is only of 14.6 months, despite the aggressive standard post-surgery treatment approaches of radiotherapy concomitant with chemotherapy with temozolomide. Altered cell metabolism has been identified as an emerging cancer hallmark, including in GB, thus offering a new target for cancer therapies. On the other hand, abnormal expression levels of miRNAs, key regulators of multiple molecular pathways, have been correlated with pathological manifestations of cancer, such…

0301 basic medicineGenetic enhancementmedicine.medical_treatmentBrain tumorAntineoplastic AgentsBiology03 medical and health sciences0302 clinical medicineDownregulation and upregulationCell MovementCell Line TumormicroRNAGeneticsmedicineHumansRNA MessengerU87Molecular BiologyGenetics (clinical)Cell ProliferationTemozolomideBrain NeoplasmsGene Expression ProfilingCancerGeneral Medicinemedicine.disease3. Good healthGene Expression Regulation NeoplasticRadiation therapyMicroRNAs030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchEnergy MetabolismGlioblastomamedicine.drugHuman Molecular Genetics
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Expression of endogenous mouse APP modulates β-amyloid deposition in hAPP-transgenic mice

2017

Amyloid-β (Aβ) deposition is one of the hallmarks of the amyloid hypothesis in Alzheimer’s disease (AD). Mouse models using APP-transgene overexpression to generate amyloid plaques have shown to model only certain parts of the disease. The extent to which the data from mice can be transferred to man remains controversial. Several studies have shown convincing treatment results in reducing Aβ and enhancing cognition in mice but failed totally in human. One model-dependent factor has so far been almost completely neglected: the endogenous expression of mouse APP and its effects on the transgenic models and the readout for therapeutic approaches. Here, we report that hAPP-transgenic models of …

0301 basic medicineGenetically modified mouseMaleMurine amyloid-betaBACE1-ASMice TransgenicPlaque Amyloidlcsh:RC346-429Pathology and Forensic Medicine03 medical and health sciencesCellular and Molecular NeuroscienceAmyloid beta-Protein Precursor0302 clinical medicineMeningesAmyloid precursor proteinMedicineAnimalsHumansTransgenic miceSenile plaqueslcsh:Neurology. Diseases of the nervous systemNeuronsAmyloid beta-Peptidesbiologybusiness.industryAmyloidosisResearchP3 peptideBrainAmyloidosismedicine.diseasePeptide FragmentsBiochemistry of Alzheimer's diseaseAstrogliosisCell biologyMice Inbred C57BL030104 developmental biologyCaspasesAmyloid precursor proteinMutationbiology.proteinAbetaFemaleNeurology (clinical)businessNeuroscienceAlzheimer’s disease030217 neurology & neurosurgery
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With mouse age comes wisdom : a review and suggestions of relevant mouse models for age-related conditions

2016

Ageing is a complex multifactorial process that results in many changes in physiological changes processes that ultimately increase susceptibility to a wide range of diseases. As such an ageing population is resulting in a pressing need for more and improved treatments across an assortment of diseases. Such treatments can come from a better understanding of the pathogenic pathways which, in turn, can be derived from models of disease. Therefore the more closely the model resembles the disease situation the more likely relevant the data will be that is generated from them. Here we review the state of knowledge of mouse models of a range of diseases and aspects of an ageing physiology that ar…

0301 basic medicineGerontologyAgingPopulation ageingProcess (engineering)TRAUMATIC BRAIN-INJURYDiseaseBiologyMouse modelsMice03 medical and health sciences0302 clinical medicineAge relatedMedicine and Health SciencesAnimalsHumansCLOSED-BONE-FRACTURESENESCENCE-ACCELERATED MOUSEE-DEFICIENT MICECELL-MEDIATED-IMMUNITYTRIPLE-TRANSGENIC MODELBiology and Life SciencesNECROSIS-FACTOR-ALPHAAged patientsCell mediated immunityC-REACTIVE PROTEINACTIVATION IN-VIVODisease Models AnimalPatient populationAgeing030104 developmental biologyAgeingPhenotypingMouse models ; ageing ; phenotypingLONG-TERM POTENTIATION030217 neurology & neurosurgeryCognitive psychologyDevelopmental Biology
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Oligodendrocytes Support Neuronal Glutamatergic Transmission via Expression of Glutamine Synthetase.

2019

Summary: Glutamate has been implicated in a wide range of brain pathologies and is thought to be metabolized via the astrocyte-specific enzyme glutamine synthetase (GS). We show here that oligodendrocytes, the myelinating glia of the central nervous system, also express high levels of GS in caudal regions like the midbrain and the spinal cord. Selective removal of oligodendrocyte GS in mice led to reduced brain glutamate and glutamine levels and impaired glutamatergic synaptic transmission without disrupting myelination. Furthermore, animals lacking oligodendrocyte GS displayed deficits in cocaine-induced locomotor sensitization, a behavior that is dependent on glutamatergic signaling in th…

0301 basic medicineGlutamineCentral nervous systemNeurotransmissionBiologyGeneral Biochemistry Genetics and Molecular BiologyArticleMidbrain03 medical and health sciencesGlutamatergic0302 clinical medicineGlutamate-Ammonia LigaseGlutamine synthetasemedicineAnimalslcsh:QH301-705.5Glutamate receptorBrainOligodendrocyteCell biologyGlutamineOligodendroglia030104 developmental biologymedicine.anatomical_structurenervous systemlcsh:Biology (General)030217 neurology & neurosurgerySignal TransductionCell reports
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Hg and Se exposure in brain tissues of striped dolphin (Stenella coeruleoalba) and bottlenose dolphin (Tursiops truncatus) from the Tyrrhenian and Ad…

2017

In this study we analyzed Hg and Se concentrations in dolphin brain tissues of fifteen specimens of striped dolphin (Stenella coeruleoalba) and eight specimens of bottlenose dolphin (Tursiops truncatus) stranded in the Tyrrhenian and Adriatic Seas, in order to assess the toxicological risks associated with Hg exposure. High Hg concentrations were found in brain tissues of both analyzed specie (1.86–243 mg/kg dw for striped dolphin and 2.1–98.7 mg/kg dw for bottlenose dolphin), exceeding levels associated with marine mammals neurotoxicity. Althougth the results clearly suggest that the protective effects of Se against Hg toxicity occur in cetaceans’ brain tissues, a molar excess of mercury w…

0301 basic medicineHealth Toxicology and MutagenesisZoologyStenella coeruleoalba010501 environmental sciencesBiologyManagement Monitoring Policy and LawToxicology01 natural sciencesAquatic organisms03 medical and health sciencesSeleniumStenellabiology.animalNeurotoxicityAnimalsSettore CHIM/01 - Chimica Analitica0105 earth and related environmental sciencesBrain; Mercury; Neurotoxicity; Selenium; Stenella coeruleoalba; Tursiops truncatus; Animals; Bottle-Nosed Dolphin; Brain; Italy; Mercury; Selenium; Stenella; Water Pollutants; Risk assessmentAnimalBrainAquatic animalGeneral MedicineMercuryBottlenose dolphinbiology.organism_classificationFisheryBottle-Nosed Dolphin030104 developmental biologyItalyStenella coeruleoalbaTursiops truncatuhuman activitiesWater Pollutants ChemicalEcotoxicology (London, England)
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Oxidative Stress-Induced Axon Fragmentation Is a Consequence of Reduced Axonal Transport in Hereditary Spastic Paraplegia SPAST Patient Neurons

2020

Hereditary spastic paraplegia (HSP) is a group of inherited disorders characterized by progressive spasticity and paralysis of the lower limbs. Autosomal dominant mutations in SPAST gene account for ∼40% of adult-onset patients. We have previously shown that SPAST patient cells have reduced organelle transport and are therefore more sensitive to oxidative stress. To test whether these effects are present in neuronal cells, we first generated 11 induced pluripotent stem (iPS) cell lines from fibroblasts of three healthy controls and three HSP patients with different SPAST mutations. These cells were differentiated into FOXG1-positive forebrain neurons and then evaluated for multiple aspects …

0301 basic medicineHereditary spastic paraplegiaOxidative phosphorylationSpastinmedicine.disease_causelcsh:RC321-57103 medical and health sciences0302 clinical medicinemedicineSPASTAxonFragmentation (cell biology)hereditary spastic paraplegialcsh:Neurosciences. Biological psychiatry. NeuropsychiatryGeneral Neuroscienceperoxisomesaxon transportmedicine.diseaseepothilone Daxon degenerationCell biology030104 developmental biologymedicine.anatomical_structurenervous systemForebrainAxoplasmic transport030217 neurology & neurosurgeryOxidative stressFrontiers in Neuroscience
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Deciphering Alzheimer’s Disease Pathogenic Pathway: Role of Chronic Brain Hypoperfusion on p-Tau and mTOR

2021

This review examines new biomolecular findings that lend support to the hemodynamic role played by chronic brain hypoperfusion (CBH) in driving a pathway to Alzheimer’s disease (AD). CBH is a common clinical feature of AD and the current topic of intense investigation in AD models. CBH is also the basis for the vascular hypothesis of AD which we originally proposed in 1993. New biomolecular findings reveal the interplay of CBH in increasing tau phosphorylation (p-Tau) in the hippocampus and cortex of AD mice, damaging fast axonal transport, increasing signaling of mammalian target of rapamycin (mTOR), impairing learning-memory function, and promoting the formation of neurofibrillary tangles…

0301 basic medicineHippocampustau ProteinsDisease03 medical and health sciences0302 clinical medicineAlzheimer DiseasemedicineAnimalsHumansCognitive declinePI3K/AKT/mTOR pathwayCerebral hypoperfusionbusiness.industryTOR Serine-Threonine KinasesGeneral NeuroscienceNeurodegenerationBrainGeneral Medicinemedicine.diseaseCortex (botany)Psychiatry and Mental healthClinical Psychology030104 developmental biologyCerebrovascular CirculationAxoplasmic transportGeriatrics and GerontologybusinessNeuroscience030217 neurology & neurosurgeryJournal of Alzheimer's Disease
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