Search results for "HALO"

showing 10 items of 2623 documents

Cerebello-cortical network fingerprints differ between essential, Parkinson's and mimicked tremors.

2017

Cerebello-thalamo-cortical loops play a major role in the emergence of pathological tremors and voluntary rhythmic movements. It is unclear whether these loops differ anatomically or functionally in different types of tremor. We compared age- and sex-matched groups of patients with Parkinson's disease or essential tremor and healthy controls (n = 34 per group). High-density 256-channel EEG and multi-channel EMG from extensor and flexor muscles of both wrists were recorded simultaneously while extending the hands against gravity with the forearms supported. Tremor was thereby recorded from patients, and voluntarily mimicked tremor was recorded from healthy controls. Tomographic maps of EEG-E…

0301 basic medicineMaleCerebellumEfferentEssential TremorSensory systemElectroencephalographyPremotor cortex03 medical and health sciences0302 clinical medicineCerebellumNeural PathwaysmedicineImage Processing Computer-AssistedHumansMuscle SkeletalAgedEssential tremorResting state fMRImedicine.diagnostic_testbusiness.industryElectromyographyMotor CortexElectroencephalographyParkinson DiseaseMiddle Agedmedicine.diseaseMagnetic Resonance Imagingnervous system diseases030104 developmental biologymedicine.anatomical_structureNonlinear DynamicsCerebral cortexCase-Control StudiesFemaleNeurology (clinical)businessNeuroscience030217 neurology & neurosurgeryBrain : a journal of neurology
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General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation.

2016

Relapsing-remitting multiple sclerosis (MS)(2) is characterized by phases of acute neuroinflammation followed by spontaneous remission. Termination of inflammation is accompanied by an influx of regulatory T cells (Tregs).(3) The molecular mechanisms responsible for directing Tregs into the inflamed CNS tissue, however, are incompletely understood. In an MS mouse model we show that the stress kinase general control non-derepressible 2 (GCN2),(4) expressed in T cells, contributes to the resolution of autoimmune neuroinflammation. Failure to recover from acute inflammation was associated with reduced frequencies of CNS-infiltrating Tregs. GCN2 deficient Tregs displayed impaired migration to a…

0301 basic medicineMaleChemokineEncephalomyelitis Autoimmune ExperimentalTime FactorsT cellImmunologyInflammationSpontaneous remissionMice TransgenicCCL2Protein Serine-Threonine KinasesT-Lymphocytes RegulatoryStatistics Nonparametric03 medical and health sciencesMice0302 clinical medicineCell MovementmedicineImmunology and AllergyAnimalsAnnexin A5NeuroinflammationbiologyKinaseMultiple sclerosisBrainEndothelial Cellsmedicine.diseaseFlow CytometryPeptide FragmentsMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesImmunologybiology.proteinDisease ProgressionCytokinesFemaleMyelin-Oligodendrocyte GlycoproteinNeurology (clinical)medicine.symptom030215 immunologyJournal of neuroimmunology
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Blimp1 Prevents Methylation of Foxp3 and Loss of Regulatory T Cell Identity at Sites of Inflammation

2018

Summary Foxp3+ regulatory T (Treg) cells restrict immune pathology in inflamed tissues; however, an inflammatory environment presents a threat to Treg cell identity and function. Here, we establish a transcriptional signature of central nervous system (CNS) Treg cells that accumulate during experimental autoimmune encephalitis (EAE) and identify a pathway that maintains Treg cell function and identity during severe inflammation. This pathway is dependent on the transcriptional regulator Blimp1, which prevents downregulation of Foxp3 expression and “toxic” gain-of-function of Treg cells in the inflamed CNS. Blimp1 negatively regulates IL-6- and STAT3-dependent Dnmt3a expression and function …

0301 basic medicineMaleEncephalomyelitis Autoimmune ExperimentalBlimp1CNS2Regulatory T cellInflammationchemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyArticleepigenetic regulationDNA Methyltransferase 3AEpigenesis Genetic03 medical and health sciencesGenomic ImprintingMice0302 clinical medicineImmune systemDownregulation and upregulationmedicineAnimalsEpigeneticsDNA (Cytosine-5-)-Methyltransferaseslcsh:QH301-705.5Regulation of gene expressionInterleukin-6FOXP3Forkhead Transcription FactorsDNA methyltransferaseshemic and immune systemsDNA Methylation3. Good healthCell biologyddc:Mice Inbred C57BL030104 developmental biologymedicine.anatomical_structureregulatory T cellslcsh:Biology (General)inflammationFoxp3DNA methylationFemalePositive Regulatory Domain I-Binding Factor 1medicine.symptomCNS030217 neurology & neurosurgeryCell Reports
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Fast direct neuronal signaling via the IL-4 receptor as therapeutic target in neuroinflammation.

2018

Ongoing axonal degeneration is thought to underlie disability in chronic neuroinflammation, such as multiple sclerosis (MS), especially during its progressive phase. Upon inflammatory attack, axons undergo pathological swelling, which can be reversible. Because we had evidence for beneficial effects of T helper 2 lymphocytes in experimental neurotrauma and discovered interleukin-4 receptor (IL-4R) expressed on axons in MS lesions, we aimed at unraveling the effects of IL-4 on neuroinflammatory axon injury. We demonstrate that intrathecal IL-4 treatment during the chronic phase of several experimental autoimmune encephalomyelitis models reversed disease progression without affecting inflamma…

0301 basic medicineMaleEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisEncephalomyelitisInflammation03 medical and health sciencesMice0302 clinical medicinemedicineAnimalsHumansAxonReceptorNeuroinflammationAdministration IntranasalInflammationNeuronsbusiness.industryMultiple sclerosisExperimental autoimmune encephalomyelitisTranslation (biology)General Medicinemedicine.diseaseAxonsReceptors Interleukin-4030104 developmental biologymedicine.anatomical_structurenervous systemInterleukin-4medicine.symptombusinessNeuroscience030217 neurology & neurosurgeryLocomotionScience translational medicine
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Lipoprotein receptor loss in forebrain radial glia results in neurological deficits and severe seizures.

2020

The Alzheimer disease-associated multifunctional low-density lipoprotein receptor-related protein-1 is expressed in the brain. Recent studies uncovered a role of this receptor for the appropriate functioning of neural stem cells, oligodendrocytes, and neurons. The constitutive knock-out (KO) of the receptor is embryonically lethal. To unravel the receptors' role in the developing brain we generated a mouse mutant by specifically targeting radial glia stem cells of the dorsal telencephalon. The low-density lipoprotein receptor-related protein-1 lineage-restricted KO female and male mice, in contrast to available models, developed a severe neurological phenotype with generalized seizures duri…

0301 basic medicineMaleEpendymoglial CellsBiology03 medical and health sciencesCellular and Molecular NeuroscienceEpilepsyMice0302 clinical medicineProsencephalonSeizuresmedicineAnimalsReceptors LipoproteinLipoprotein receptor-related proteinmedicine.diseaseNeural stem cellLipoproteins LDL030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesTissue Plasminogen ActivatorForebrainFemaleSynaptic signalingStem cellPostsynaptic densityNeuroscience030217 neurology & neurosurgeryAstrocyteGliaREFERENCES
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Somatosensory Brain Function and Gray Matter Regional Volumes Differ According to Exercise History : Evidence from Monozygotic Twins

2017

Associations between long-term physical activity and cortical function and brain structure are poorly known. Our aim was to assess whether brain functional and/or structural modulation associated with long-term physical activity is detectable using a discordant monozygotic male twin pair design. Nine monozygotic male twin pairs were carefully selected for an intrapair difference in their leisure-time physical activity of at least three years duration (mean age 34 ± 1 years). We registered somatosensory mismatch response (SMMR) in EEG to electrical stimulation of fingers and whole brain MR images. We obtained exercise history and measured physical fitness and body composition. Equivalent ele…

0301 basic medicineMaleFITNESSMismatch negativityphysical activityMismatch negativityElectroencephalographycomputer.software_genreSomatosensory systemSuperior temporal gyrus0302 clinical medicineVoxelBrain structureGENERATORSTwin researchGray MatterRadiological and Ultrasound Technologymedicine.diagnostic_testOrgan SizeMagnetic Resonance Imaging3142 Public health care science environmental and occupational healthmedicine.anatomical_structureNeurologyEXCITABILITYHEALTHAnatomyPsychologyAdultsomatosensory cortexMISMATCH NEGATIVITY MMNPOTENTIALS03 medical and health sciencesTIME PHYSICAL-ACTIVITYmedicineBrain electrophysiologyHumansRadiology Nuclear Medicine and imagingMODULATIONExercisekaksostutkimusbrain electrophysiologyPostcentral gyrusPhysical activitybrain structureTwins MonozygoticMedial frontal gyrusTwin studySomatosensory cortex030104 developmental biologyDISCRIMINATIONNeurology (clinical)poikkeavuusnegatiivisuuscomputerNeuroscience030217 neurology & neurosurgeryRESPONSES
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IQSEC2-related encephalopathy in males and females: a comparative study including 37 novel patients.

2019

Variants in IQSEC2, escaping X inactivation, cause X-linked intellectual disability with frequent epilepsy in males and females. We aimed to investigate sex-specific differences.

0301 basic medicineMaleGénétique clinique[SDV]Life Sciences [q-bio]MedizinPhysiology030105 genetics & hereditySeizures/epidemiologyEpilepsyBrain Diseases/epidemiologyX-linked inheritanceIntellectual disabilityGuanine Nucleotide Exchange FactorsProtein IsoformsMissense mutationGenetics(clinical)10. No inequalityNon-U.S. Gov'tGenetics (clinical)X-linked recessive inheritanceComputingMilieux_MISCELLANEOUSBrain DiseasesSex CharacteristicsResearch Support Non-U.S. Gov'tBrainSciences bio-médicales et agricoles3. Good healthPedigreePhenotypeintellectual disabilityFemaleBrain/growth & developmentSex characteristicsGénétique moléculaireGuanine Nucleotide Exchange Factors/geneticsEncephalopathyResearch SupportX-inactivationArticle03 medical and health sciencesSeizuresProtein Isoforms/geneticsmedicineJournal ArticleIQSEC2HumansIntellectual Disability/epidemiology[SDV.GEN]Life Sciences [q-bio]/Geneticsbusiness.industryInfant NewbornisoformsCorrectionInfantmedicine.diseaseNewbornHuman genetics030104 developmental biologyMutationepilepsyHuman medicinebusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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PRRT2 gene variant in a child with dysmorphic features, congenital microcephaly, and severe epileptic seizures: genotype-phenotype correlation?

2019

Abstract Background Mutations in Proline-rich Transmembrane Protein 2 (PRRT2) have been primarily associated with individuals presenting with infantile epilepsy, including benign familial infantile epilepsy, benign infantile epilepsy, and benign myoclonus of early infancy, and/or with dyskinetic paroxysms such as paroxysmal kinesigenic dyskinesia, paroxysmal non-kinesigenic dyskinesia, and exercise-induced dyskinesia. However, the clinical manifestations of this disorder vary widely. PRRT2 encodes a protein expressed in the central nervous system that is mainly localized in the pre-synaptic neurons and is involved in the modulation of synaptic neurotransmitter release. The anomalous functio…

0301 basic medicineMaleMicrocephalyMutation MissenseCase ReportNerve Tissue ProteinsBioinformaticsRisk AssessmentSeverity of Illness Index03 medical and health sciences0302 clinical medicineRare DiseasesSeizuresmedicineHumansGenetic Predisposition to DiseaseGenetic TestingExome sequencingGenetic Association StudiesBenign familial infantile epilepsyDysmorphic featuresbusiness.industryEpileptic encephalopathylcsh:RJ1-570InfantMembrane Proteinslcsh:PediatricsParoxysmal dyskinesiamedicine.diseaseBody Dysmorphic DisordersPrognosisPRRT2 mutationMagnetic Resonance Imaging030104 developmental biologyDyskinesiaMicrocephalymedicine.symptomPRRT2 mutation Dysmorphic features Microcephaly Epileptic encephalopathybusinessMyoclonus030217 neurology & neurosurgeryPRRT2Benign infantile epilepsy
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Dopamine neurons drive fear extinction learning by signaling the omission of expected aversive outcomes

2018

Extinction of fear responses is critical for adaptive behavior and deficits in this form of safety learning are hallmark of anxiety disorders. However, the neuronal mechanisms that initiate extinction learning are largely unknown. Here we show, using single-unit electrophysiology and cell-type specific fiber photometry, that dopamine neurons in the ventral tegmental area (VTA) are activated by the omission of the aversive unconditioned stimulus (US) during fear extinction. This dopamine signal occurred specifically during the beginning of extinction when the US omission is unexpected, and correlated strongly with extinction learning. Furthermore, temporally-specific optogenetic inhibition o…

0301 basic medicineMaleMouseExtinction PsychologicalPhotometry0302 clinical medicineFear conditioningBiology (General)extinctionGeneral NeuroscienceQRElectroencephalographyGeneral MedicineFearmusculoskeletal systemhumanitiesVentral tegmental areamedicine.anatomical_structureMedicineAnxietymedicine.symptomdopaminePsychologygeographic locationsmedicine.drugResearch ArticleQH301-705.5ScienceOptogeneticsUnconditioned stimulussafety learningGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesextinction ; fear conditioning ; safety learning ; dopamineDopaminemedicineAvoidance LearningAnimalsLearningddc:610General Immunology and MicrobiologyDopaminergic NeuronsVentral Tegmental AreaExtinction (psychology)social sciencesfear conditioningMice Inbred C57BLOptogeneticsElectrophysiology030104 developmental biologyNeuroscience030217 neurology & neurosurgeryNeuroscience
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The Cumulative Effect of Transient Synchrony States on Motor Performance in Parkinson's Disease.

2020

Bursts of beta frequency band activity in the basal ganglia of patients with Parkinson's disease (PD) are associated with impaired motor performance. Here we test in human adults whether small variations in the timing of movement relative to beta bursts have a critical effect on movement velocity and whether the cumulative effects of multiple beta bursts, both locally and across networks, matter.

0301 basic medicineMaleParkinson's diseaseBehavioral/CognitiveParkinson's diseaseDeep Brain StimulationElectroencephalography Phase Synchronization610 Medicine & healthLocal field potentialHypokinesialocal field potentialsBasal Ganglia03 medical and health sciencesBursting0302 clinical medicineSubthalamic NucleusBasal gangliaMedicineHumansBeta (finance)610 Medicine & healthCumulative effectResearch ArticlesAgedCued speechbeta oscillationsbusiness.industryGeneral NeuroscienceParkinson DiseaseMiddle Agedmedicine.diseaseSubthalamic nucleus030104 developmental biologyFemaleCuesbusinessBeta RhythmNeuroscience030217 neurology & neurosurgeryPhotic StimulationPsychomotor Performance
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