Search results for "Neuropathology"

showing 10 items of 43 documents

Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension

2020

Arterial hypertension is the most important risk factor for the development of cardiovascular disease. Recently, aircraft noise has been shown to be associated with elevated blood pressure, endothelial dysfunction, and oxidative stress. Here, we investigated the potential exacerbated cardiovascular effects of aircraft noise in combination with experimental arterial hypertension. C57BL/6J mice were infused with 0.5 mg/kg/d of angiotensin II for 7 days, exposed to aircraft noise for 7 days at a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A), or subjected to both stressors. Noise and angiotensin II increased blood pressure, endothelial dysfunction, oxidati…

0301 basic medicineAircraftmedicine.medical_treatmentClinical BiochemistryBlood Pressure1308 Clinical Biochemistrymedicine.disease_causeBiochemistryMice0302 clinical medicineMedicineEndothelial dysfunctionlcsh:QH301-705.5lcsh:R5-920NADPH oxidasebiologyCytokineHypertensionmedicine.symptomlcsh:Medicine (General)Arterial hypertensionmedicine.medical_specialtyArticles from the Special Issue on Impact of environmental pollution and stress on redox signaling and oxidative stress pathways; Edited by Thomas Münzel and Andreas Daiber10208 Institute of Neuropathology610 Medicine & healthInflammation03 medical and health sciencesInternal medicineEnvironmental noise exposureAnimalsNeuroinflammationInflammationbusiness.industryOrganic ChemistryEndothelial functionmedicine.diseaseAngiotensin IIMice Inbred C57BLOxidative Stress030104 developmental biologyEndocrinologyBlood pressurelcsh:Biology (General)Vascular oxidative stressbiology.protein570 Life sciences; biologyEndothelium Vascularbusiness030217 neurology & neurosurgeryOxidative stress1605 Organic ChemistryRedox Biology
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Epilepsy in neuropathologically verified Alzheimer's disease.

2018

Abstract Purpose Subjects with Alzheimer's disease (AD) have been shown to be at a higher risk for epilepsy. The vast majority of the previous studies have not included a full neuropathological examination. Methods The objective of this study was to assess the prevalence of epilepsy and clinicopathological characteristics in a well-defined study group of 64 subjects with AD. We evaluated the clinicopathological findings in 64 subjects (mean age at death 85 ± 8.6 years) from a longitudi-nal study cohort of patients with dementia. Results Eleven out of the 64 subjects (17%) had a history of epilepsy, which is comparable to previous studies. The subjects with AD and epilepsy were significantly…

0301 basic medicineApolipoprotein EMalemedicine.medical_specialtyNeurologyTime FactorsalzheimerAutopsyNeuropathologyDiseaseAlzheimerin tauti03 medical and health sciencesEpilepsyautopsy0302 clinical medicineApolipoproteins EAlzheimer DiseaseInternal medicinemedicinePrevalenceDementiaHumansneurodegenerative diseasesLongitudinal Studiesta515ta316Aged 80 and overEpilepsybusiness.industryneurodegenerationAge FactorsBrainGeneral MedicineAlzheimer's diseasemedicine.diseaseneurodegeneratiiviset sairaudetHospitalization030104 developmental biologyNeurologyruumiinavausCohortFemaleNeurology (clinical)businessepilepsia030217 neurology & neurosurgerydementiaFollow-Up StudiesSeizure
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Role of Microbiota-Derived Extracellular Vesicles in Gut-Brain Communication

2021

Human intestinal microbiota comprise of a dynamic population of bacterial species and other microorganisms with the capacity to interact with the rest of the organism and strongly influence the host during homeostasis and disease. Commensal and pathogenic bacteria coexist in homeostasis with the intestinal epithelium and the gastrointestinal tract’s immune system, or GALT (gut-associated lymphoid tissue), of the host. However, a disruption to this homeostasis or dysbiosis by different factors (e.g., stress, diet, use of antibiotics, age, inflammatory processes) can cause brain dysfunction given the communication between the gut and brain. Recently, extracellular vesicles (EVs) derived from …

0301 basic medicineLipopolysaccharideQH301-705.5brainReviewBiologymedicine.disease_causeCatalysisInorganic ChemistryNeuroblastoma03 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmune systemmedicinemicrobiotaAnimalsHumansPhysical and Theoretical ChemistryBiology (General)ReceptorbacteriaMolecular BiologyQD1-999SpectroscopyGastrointestinal tractneuropathologyOrganic ChemistryPathogenic bacteriaGeneral Medicinemedicine.diseaseIntestinal epitheliumComputer Science ApplicationsCell biologyChemistry030104 developmental biologychemistryRNA Long Noncodingextracellular vesiclesDysbiosis030217 neurology & neurosurgeryHomeostasisInternational Journal of Molecular Sciences
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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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Bi-allelic JAM2 Variants Lead to Early-Onset Recessive Primary Familial Brain Calcification

2020

International audience; Primary familial brain calcification (PFBC) is a rare neurodegenerative disorder characterized by a combination of neurological, psychiatric, and cognitive decline associated with calcium deposition on brain imaging. To date, mutations in five genes have been linked to PFBC. However, more than 50% of individuals affected by PFBC have no molecular diagnosis. We report four unrelated families presenting with initial learning difficulties and seizures and later psychiatric symptoms, cerebellar ataxia, extrapyramidal signs, and extensive calcifications on brain imaging. Through a combination of homozygosity mapping and exome sequencing, we mapped this phenotype to chromo…

0301 basic medicineMaleCerebellumPathology[SDV]Life Sciences [q-bio]recessive brain calcificationMice0302 clinical medicineCognitive declineAge of OnsetChildGenetics (clinical)Exome sequencingComputingMilieux_MISCELLANEOUSBrain Diseasesprimary familial brain calcificationMalalties neurodegenerativesBrainFahr diseaseCalcinosisOCLNNeurodegenerative DiseasesHuman brainMiddle AgedPedigree[SDV] Life Sciences [q-bio]medicine.anatomical_structureKnockout mouseFemalemedicine.symptomAdultmedicine.medical_specialtyAdolescentGenes RecessiveNeuropathologyBiologyCalcificacióCalcification03 medical and health sciencesBasal Ganglia DiseasesReportGeneticsmedicineAnimalsHumansAllelesSLC20A2Cerebellar ataxiaknock out mouse modelmedicine.diseaseJAM2030104 developmental biologyFahr disease; familial idiopathic basal ganglia calcification; JAM2; JAM3; knock out mouse model; MYORG; OCLN; primary familial brain calcification; recessive brain calcification; SLC20A2familial idiopathic basal ganglia calcificationJAM3MYORGXenotropic and Polytropic Retrovirus ReceptorCell Adhesion Molecules030217 neurology & neurosurgeryCalcification
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Autoantibodies Profile in Matching CSF and Serum from AD and aMCI patients: Potential Pathogenic Role and Link to Oxidative Damage.

2015

Abstract Alzheimer disease (AD) is the most common form of dementia among the elderly and is characterized by progressive loss of memory and cognition. Amyloid-s-peptide (As) forms senile plaques, which, together with hyperphosphorylated tau-based neurofibrillary tangles, are the hallmarks of AD neuropathology. Evidence support the involvement of immune system in AD progression and current concepts regarding its pathogenesis include the participation of inflammatory and autoimmune components in the neurodegenerative process. Pathologically, immune system components have been detected in the brain, cerebrospinal fluid (CSF) and in serum of AD subjects and their trend of variation correlates …

0301 basic medicineMalePathologymedicine.medical_specialtyBlotting WesternNeuropathologyaged; aged 80 and over; alzheimer disease; autoantibodies; biomarkers; blotting western; cognitive dysfunction; female; frontal lobe; humans; male; mass spectrometry; oxidative stressmedicine.disease_causeMass SpectrometryAutoimmunity03 medical and health sciences0302 clinical medicineCerebrospinal fluidImmune systemAlzheimer DiseasemedicineDementiaHumansCognitive DysfunctionSenile plaquesAgedAutoantibodiesAged 80 and overAutoantibodymedicine.diseaseFrontal LobeOxidative Stress030104 developmental biologyNeurologyImmunologyFemaleNeurology (clinical)Alzheimer's diseasePsychology030217 neurology & neurosurgeryBiomarkersCurrent Alzheimer research
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Functional Improvement after Photothrombotic Stroke in Rats Is Associated with Different Patterns of Dendritic Plasticity after G-CSF Treatment and G…

2016

We have previously shown that granulocyte-colony stimulating factor (G-CSF) treatment alone, or in combination with constraint movement therapy (CIMT) either sequentially or concomitantly, results in significantly improved sensorimotor recovery after photothrombotic stroke in rats in comparison to untreated control animals. CIMT alone did not result in any significant differences compared to the control group (Diederich et al., Stroke, 2012;43:185-192). Using a subset of rat brains from this former experiment the present study was designed to evaluate whether dendritic plasticity would parallel improved functional outcomes. Five treatment groups were analyzed (n = 6 each) (i) ischemic contr…

0301 basic medicineMalemedicine.medical_specialtyLightmedicine.medical_treatmentMovement10208 Institute of NeuropathologyIschemialcsh:Medicine610 Medicine & health1100 General Agricultural and Biological Sciences03 medical and health sciences0302 clinical medicine1300 General Biochemistry Genetics and Molecular BiologyInternal medicineNeuroplasticityGranulocyte Colony-Stimulating FactormedicineAnimalscardiovascular diseasesRats Wistarlcsh:ScienceSalineStrokePhysical Therapy Modalities1000 MultidisciplinaryMultidisciplinaryNeuronal Plasticitybusiness.industryPyramidal Cellslcsh:RDendritesRecovery of Functionmedicine.diseaseCombined Modality TherapyCortex (botany)SurgeryGranulocyte colony-stimulating factorConstraint-induced movement therapyStroke030104 developmental biologyEndocrinologyConcomitant570 Life sciences; biologylcsh:Qbusiness030217 neurology & neurosurgeryResearch ArticlePLoS ONE
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Two different pathogenic mechanisms, dying-back axonal neuropathy and pancreatic senescence, are present in the YG8R mouse model of Friedreich ataxia

2016

Frataxin (FXN) deficiency causes Friedreich's ataxia (FRDA), a multisystem disorder with neurological and non-neurological symptoms. FRDA pathophysiology combines developmental and degenerative processes of dorsal root ganglia (DRG), sensory nerves, dorsal columns and other central nervous structures. A dying-back mechanism has been proposed to explain the peripheral neuropathy and neuropathology. In addition, affected individuals have non-neuronal symptoms such as diabetes mellitus or glucose intolerance. To go further in the understanding of the pathogenic mechanisms of neuropathy and diabetes associated with the disease, we have investigated the humanized mouse YG8R model of FRDA. By bio…

0301 basic medicineNervous systemAgingPathologylcsh:MedicineMedicine (miscellaneous)Mice0302 clinical medicineImmunology and Microbiology (miscellaneous)Ganglia SpinalInsulin-Secreting CellsInsulin SecretionInsulinMuscle spindleDorsal root gangliaCellular SenescenceDiabetisbiologyMusclesDiabetesAnatomyMitochondria3. Good healthmedicine.anatomical_structureSistema nerviós simpàticDying-back neuropathyPeripheral nervous systemCell senescencemedicine.symptomOxidation-Reductionlcsh:RB1-214Research ArticleSenescencemedicine.medical_specialtyAtaxiaNeuroscience (miscellaneous)Friedreich’s ataxiaNeuropathologyGeneral Biochemistry Genetics and Molecular BiologyPàncreesMalalties del sistema nerviós03 medical and health sciencesPeripheral Nervous Systemlcsh:PathologymedicineAnimalsHumansPancreasIslet of Langerhanslcsh:R302Friedreich's ataxiaNervous system Diseasesmedicine.diseaseAxonsMice Inbred C57BLDisease Models Animal030104 developmental biologyPeripheral neuropathyFriedreich AtaxiaSympathetic nervous systemMutationHumanized mouseFrataxinbiology.proteinEnergy Metabolism030217 neurology & neurosurgeryDisease Models & Mechanisms
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Septin/anillin filaments scaffold central nervous system myelin to accelerate nerve conduction

2016

Myelination of axons facilitates rapid impulse propagation in the nervous system. The axon/myelin-unit becomes impaired in myelin-related disorders and upon normal aging. However, the molecular cause of many pathological features, including the frequently observed myelin outfoldings, remained unknown. Using label-free quantitative proteomics, we find that the presence of myelin outfoldings correlates with a loss of cytoskeletal septins in myelin. Regulated by phosphatidylinositol-(4,5)-bisphosphate (PI(4,5)P2)-levels, myelin septins (SEPT2/SEPT4/SEPT7/SEPT8) and the PI(4,5)P2-adaptor anillin form previously unrecognized filaments that extend longitudinally along myelinated axons. By confoca…

0301 basic medicineNervous systemCentral Nervous SystemProteomicsScaffoldMouseProteomeNeural ConductionSeptinNerve Fibers MyelinatedMyelinGene Knockout TechniquesMiceContractile ProteinsAxonBiology (General)CytoskeletonMicroscopy ImmunoelectronCytoskeletonMyelin SheathMicroscopy ConfocalGeneral NeuroscienceQRGeneral MedicineAnatomyCell biologyglial cellsmedicine.anatomical_structureGene TargetingMedicineResearch ArticleQH301-705.5ScienceCentral nervous systemmyelinated axonsmacromolecular substancesBiologyGeneral Biochemistry Genetics and Molecular Biologymyelin structure03 medical and health sciencesSeptin/anillin filaments; central nervous system; myelinlabel-free proteomicsmedicineAnimalsneuropathologyGeneral Immunology and Microbiology030104 developmental biologynervous systemseptin cytoskeletonProtein MultimerizationSeptinsSeptin cytoskeletonNeuroscienceeLife
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Exosomes as mediators of neuron-glia communication in neuroinflammation

2019

In recent years, a type of extracellular vesicles named exosomes has emerged that play an important role in intercellular communication under physiological and pathological conditions. These nanovesicles (30–150 nm) contain proteins, RNAs and lipids, and their internalization by bystander cells could alter their normal functions. This review focuses on recent knowledge about exosomes as messengers of neuron-glia communication and their participation in the physiological and pathological functions in the central nervous system. Special emphasis is placed on the role of exosomes under toxic or pathological stimuli within the brain, in which the glial exosomes containing inflammatory molecules…

0301 basic medicinemedia_common.quotation_subjectCentral nervous systemneuronsReviewexosomesBiologyExosomelcsh:RC346-429neuroinflammationPathogenesis03 medical and health sciences0302 clinical medicineDevelopmental NeuroscienceBystander effectmedicineInternalizationNeuroinflammationlcsh:Neurology. Diseases of the nervous systemmedia_commonbiomarkers; exosomes; glial cells; neuroinflammation; neuron-glia commuication; neurons; neuropathology; therapyneuropathologytherapyneuron-glia commuicationbiomarkersMicrovesiclesglial cells030104 developmental biologymedicine.anatomical_structureNeuronNeuroscience030217 neurology & neurosurgeryNeural Regeneration Research
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