Search results for "BLOOD-BRAIN BARRIER"

showing 10 items of 141 documents

The Blood-Brain Barrier in Alzheimer’s Disease

2020

The accumulation of neurotoxic amyloid-beta (Aβ) in the brain is one of the characteristic hallmarks of Alzheimer's disease (AD). Aβ-peptide brain homeostasis is governed by its production and various clearance mechanisms. The blood-brain barrier provides a large surface area for influx and efflux mechanisms into and out of the brain. Different transporters and receptors have been implicated to play crucial roles in Aβ clearance from brain. Besides Aβ transport, the blood-brain barrier tightly regulates the brain's microenvironment; however, vascular alterations have been shown in patients with AD. Here, we summarize how the blood-brain barrier changes during aging and in disease and focus …

0301 basic medicineAmyloid beta-PeptidesChemistryBrainATP-binding cassette transporterTransporterBlood–brain barrierLRP1ArticlePeptide Fragments03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structureReceptors LDLAlzheimer DiseaseBlood-Brain BarriermedicineHumansEffluxReceptorNeuroscience030217 neurology & neurosurgeryHomeostasisLipoprotein
researchProduct

Numerous Fasciola plasminogen-binding proteins may underlie blood-brain barrier leakage and explain neurological disorder complexity and heterogeneit…

2019

15 páginas, 5 figuras y 1 tabla

0301 basic medicineAntifibrinolyticContact systemmedicine.drug_classmedicine.medical_treatment030231 tropical medicineBradykininInflammationNeurological disorderFibrinolysis systemProteomic and mass spectrometry analysesBlood–brain barrierFasciola excretome/secretomeProinflammatory cytokine03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBlood-brain barrier leakageFibrinolysismedicineIndicators and preventionAcute and chronic phasesPlasminogen-binding proteinsFasciolabiologyHuman fascioliasis030108 mycology & parasitologymedicine.diseasebiology.organism_classificationInfectious Diseasesmedicine.anatomical_structurechemistryImmunologyAnimal Science and ZoologyParasitologymedicine.symptomNeurological disordersResearch Article
researchProduct

Ticket to Ride: Targeting Proteins to Exosomes for Brain Delivery.

2017

Exosomes represent an attractive vehicle for the delivery of biomolecules. However, mechanisms for loading functional molecules into exosomes are relatively unexplored. Here we report the use of the evolutionarily conserved late-domain (L-domain) pathway as a mechanism for loading exogenous proteins into exosomes. We demonstrate that labeling of a target protein, Cre recombinase, with a WW tag leads to recognition by the L-domain-containing protein Ndfip1, resulting in ubiquitination and loading into exosomes. Our results show that Ndfip1 expression acts as a molecular switch for exosomal packaging of WW-Cre that can be suppressed using the exosome inhibitor GW4869. When taken up by floxed …

0301 basic medicineBiocompatibilityRecombinant Fusion ProteinsGene ExpressionComputational biologyBiologyExosomesPermeabilityCell LineExtracellular VesiclesMice03 medical and health sciencesDrug Delivery SystemsDrug DiscoveryGeneticsAnimalsMolecular BiologyPharmacologyIntegrasesbusiness.industryImmunogenicityMembrane ProteinsRNABrainProteinsMicrovesiclesBiotechnologyProtein Transport030104 developmental biologyTargeted drug deliveryBlood-Brain BarrierCommentaryMolecular MedicineOriginal ArticleNasal AbsorptionCarrier ProteinsGenetic EngineeringbusinessMolecular therapy : the journal of the American Society of Gene Therapy
researchProduct

Vascular pathology: Cause or effect in Alzheimer disease?

2018

Introduction: Alzheimer disease (AD) is the main cortical neurodegenerative disease. The incidence of this disease increases with age, causing significant medical, social and economic problems, especially in countries with ageing populations. Objective: This review aims to highlight existing evidence of how vascular dysfunction may contribute to cognitive impairment in AD, as well as the therapeutic possibilities that might arise from this evidence. Development: The vascular hypothesis emerged as an alternative to the amyloid cascade hypothesis as an explanation for the pathophysiology of AD. This hypothesis locates blood vessels as the origin for a variety of pathogenic pathways that lead …

0301 basic medicineContext (language use)DiseaseBlood–brain barrierlcsh:RC346-42903 medical and health sciences0302 clinical medicineAlzheimer DiseaseMaterials ChemistrymedicineDementiaHumanslcsh:Neurology. Diseases of the nervous systemNeuronsAmyloid beta-PeptidesVascular diseaseNeurodegenerationBrainmedicine.disease030104 developmental biologymedicine.anatomical_structureAgeingBlood-Brain BarrierCerebrovascular CirculationAlzheimer's diseasePsychologyNeuroscience030217 neurology & neurosurgeryNeurología (English Edition)
researchProduct

EGFL7 - a potential therapeutic target for multiple sclerosis?

2018

0301 basic medicineEGF Family of ProteinsMultiple SclerosisClinical BiochemistryEndothelial Growth FactorsBlood–brain barrier03 medical and health sciences0302 clinical medicineDrug DiscoveryMedicineAnimalsHumansMolecular Targeted TherapyPharmacologybusiness.industryMultiple sclerosisNatalizumabCalcium-Binding Proteinsmedicine.disease030104 developmental biologymedicine.anatomical_structureBlood-Brain BarrierMolecular MedicineEGFL7businessNeuroscience030217 neurology & neurosurgeryExpert opinion on therapeutic targets
researchProduct

Molecular Biology of Atherosclerotic Ischemic Strokes

2020

Among the causes of global death and disability, ischemic stroke (also known as cerebral ischemia) plays a pivotal role, by determining the highest number of worldwide mortality, behind cardiomyopathies, affecting 30 million people. The etiopathogenetic burden of a cerebrovascular accident could be brain ischemia (~80%) or intracranial hemorrhage (~20%). The most common site when ischemia occurs is the one is perfused by middle cerebral arteries. Worse prognosis and disablement consequent to brain damage occur in elderly patients or affected by neurological impairment, hypertension, dyslipidemia, and diabetes. Since, in the coming years, estimates predict an exponential increase of people w…

0301 basic medicineInflammasomesCerebral arteriesmicrogliaDiseaseReviewneuroinflammationBrain ischemialcsh:Chemistry0302 clinical medicineatherosclerosiStrokelcsh:QH301-705.5SpectroscopymicroRNAGeneral MedicineMKEYDKK-3Computer Science ApplicationsmicroRNAsBlood-Brain BarrierCardiologymedicine.symptomDectin-1medicine.medical_specialtyIschemiaBrain damageCatalysisInorganic Chemistry03 medical and health sciencesInternal medicineDiabetes mellitusmedicineischemic strokeAnimalsHumansPhysical and Theoretical ChemistryMolecular Biologybusiness.industryOrganic ChemistryAFmedicine.diseaseImmunity InnateNLRP3 inflammasome030104 developmental biologylcsh:Biology (General)lcsh:QD1-999atherosclerosisbusinessBBB030217 neurology & neurosurgeryDyslipidemiaCD200-CD200R
researchProduct

The Impact of Small Extracellular Vesicles on Lymphoblast Trafficking across the Blood-Cerebrospinal Fluid Barrier In Vitro.

2020

Central nervous System (CNS) disease in pediatric acute lymphoblastic leukemia (ALL) is a major concern, but still, cellular mechanisms of CNS infiltration are elusive. The choroid plexus (CP) is a potential entry site, and, to some extent, invasion resembles CNS homing of lymphocytes during healthy state. Given exosomes may precondition target tissue, the present work aims to investigate if leukemia-derived exosomes contribute to a permissive phenotype of the blood-cerebrospinal fluid barrier (BCSFB). Leukemia-derived exosomes were isolated by ultracentrifugation from the cell lines SD-1, Nalm-6, and P12-Ichikawa (P12). Adhesion and uptake to CP epithelial cells and the significance on sub…

0301 basic medicineIntegrinexosomesEndocytosisExosomecentral nervous system infiltrationCatalysisArticlepediatric acute lymphoblastic leukemiaInorganic Chemistrylcsh:Chemistry03 medical and health sciencesExtracellular Vesicles0302 clinical medicineCell MovementCentral Nervous System DiseasesCell Line TumorCell AdhesionAnimalsHumansNeoplasm InvasivenessLymphocytesPhysical and Theoretical ChemistryMolecular Biologylcsh:QH301-705.5Spectroscopychoroid plexusbiologyChemistryLymphoblastOrganic ChemistryEpithelial CellsGeneral MedicinePrecursor Cell Lymphoblastic Leukemia-LymphomaHematopoietic Stem CellsMicrovesiclesEndocytosisComputer Science ApplicationsCell biologyProtein Transport030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Cell cultureBlood-Brain Barrier030220 oncology & carcinogenesisbiology.proteinChoroid plexusHoming (hematopoietic)International journal of molecular sciences
researchProduct

The concerted amyloid-beta clearance of LRP1 and ABCB1/P-gp across the blood-brain barrier is linked by PICALM

2018

The accumulation of neurotoxic amyloid-beta (Aβ) in the brain is a characteristic hallmark of Alzheimer's disease (AD). The blood-brain barrier (BBB) provides a large surface area and has been shown to be an important mediator for removal of brain Aβ. Both, the ABC transporter P-glycoprotein (ABCB1/P-gp) and the receptor low-density lipoprotein receptor-related protein 1 (LRP1) have been implicated to play crucial roles in Aβ efflux from brain. Here, with immunoprecipitation experiments, co-immunostainings and dual inhibition of ABCB1/P-gp and LRP1, we show that both proteins are functionally linked, mediating a concerted transcytosis of Aβ through endothelial cells. Late-onset AD risk fact…

0301 basic medicineMaleAmyloid betaSwineImmunologyPrimary Cell CultureATP-binding cassette transporterBlood–brain barrierClathrinArticlePICALM03 medical and health sciencesBehavioral NeuroscienceMice0302 clinical medicineAlzheimer DiseasemedicineAnimalsATP Binding Cassette Transporter Subfamily B Member 1Mice KnockoutAmyloid beta-PeptidesbiologyEndocrine and Autonomic SystemsChemistryTumor Suppressor ProteinsPhosphatidylinositol bindingBrainEndothelial CellsLRP1Peptide FragmentsCell biologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureTranscytosisReceptors LDLBlood-Brain BarrierMonomeric Clathrin Assembly Proteinsbiology.proteinTranscytosis030217 neurology & neurosurgeryLow Density Lipoprotein Receptor-Related Protein-1Brain, Behavior, and Immunity
researchProduct

Endothelial Dab1 signaling orchestrates neuro-glia-vessel communication in the central nervous system.

2018

Developing the bloodbrain barrier During development, signals need to be dynamically integrated by endothelial cells, neurons, and glia to achieve functional neuro-glia-vascular units in the central nervous system. During cortical development, neuronal Dab1 and ApoER2 receptors respond to a guidance cue called reelin. Studying mice, Segarra et al. found that Dab1 and ApoER2 are also expressed in endothelial cells (see the Perspective by Thomas). The integration of reelin signaling in endothelial cells and neurons facilitates the communication between vessels, glia, and neurons that is necessary for the correct positioning of neurons during cortical development. This integration is also impo…

0301 basic medicineMaleCell signalingLow-density lipoprotein receptor-related protein 8EndotheliumCell Adhesion Molecules NeuronalCentral nervous systemNeovascularization PhysiologicNerve Tissue ProteinsCell Communication03 medical and health sciencesMiceCell MovementmedicineAnimalsReelinLDL-Receptor Related ProteinsCerebral CortexMice KnockoutNeuronsRetinaExtracellular Matrix ProteinsMultidisciplinarybiologyIntegrin beta1Serine EndopeptidasesRetinal VesselsDAB1Reelin Protein030104 developmental biologymedicine.anatomical_structurenervous systemCerebral cortexBlood-Brain Barrierbiology.proteinFemaleEndothelium VascularLamininNeuroscienceNeurogliaGene DeletionSignal TransductionScience (New York, N.Y.)
researchProduct

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
researchProduct