2024
The role of parvalbumin interneuron dysfunction across neurodegenerative dementias
Smeralda C, Pandit S, Turrini S, Reilly J, Palmisano A, Sprugnoli G, Hampel H, Benussi A, Borroni B, Press D, Rotenberg A, El Fakhri G, Koch G, Rossi S, Santarnecchi E. The role of parvalbumin interneuron dysfunction across neurodegenerative dementias. Ageing Research Reviews 2024, 101: 102509. PMID: 39306248, DOI: 10.1016/j.arr.2024.102509.Peer-Reviewed Original ResearchInterneuron dysfunctionCortical hyperexcitabilityTherapeutic targetCortical excitation/inhibition balanceRhythm disruptionFast-spikingPV+ cellsBasket neuronsPotential therapeutic targetInhibitory interneuronsExcitation/inhibition balanceOscillatory disruptionsSymptom onsetNovel biomarkersHyperexcitabilityDysfunctionNeuronal deathOscillatory activityDementia with Lewy bodiesPathophysiological frameworkClinical symptom onsetFrontotemporal dementia
2023
Cortical GABA Levels Are Reduced in Post-Acute COVID-19 Syndrome
Marinkovic K, White D, Myers A, Parker K, Arienzo D, Mason G. Cortical GABA Levels Are Reduced in Post-Acute COVID-19 Syndrome. Brain Sciences 2023, 13: 1666. PMID: 38137114, PMCID: PMC10741691, DOI: 10.3390/brainsci13121666.Peer-Reviewed Original ResearchAcute COVID-19 illnessCOVID-19 illnessGABA levelsN-acetylaspartatePost-acute COVID-19 syndromeCortical GABA levelsPersistent cognitive dysfunctionPost-acute sequelaeCOVID-19 syndromeExcitation/inhibition imbalancePoor sleep qualityProton magnetic resonance spectroscopyDepression/anxietyQuality of lifePersistent neuroinflammationBrain fogCortical hyperexcitabilityLong COVIDAlcohol intakeCognitive dysfunctionNeuronal integrityNeurocognitive dysfunctionNeurochemical aspectsSleep qualityOccipital cortexThe clinical and genomic features of seizures in meningiomas
Dincer A, Jalal M, Gupte T, Vetsa S, Vasandani S, Yalcin K, Marianayagam N, Blondin N, Corbin Z, McGuone D, Fulbright R, Erson-Omay Z, Günel M, Moliterno J. The clinical and genomic features of seizures in meningiomas. Neuro-Oncology Advances 2023, 5: i49-i57. PMID: 37287582, PMCID: PMC10243847, DOI: 10.1093/noajnl/vdac110.Peer-Reviewed Original ResearchPeritumoral brain edemaPostoperative seizuresBrain invasionSubtotal resectionBrain edemaLarge residual tumor volumeCentral nervous system tumorsCommon central nervous system tumorPersistent postoperative seizuresResidual tumor volumeHistory of seizuresHigh tumor gradeNervous system tumorsQuality of lifePreoperative seizuresAtypical histologyMost patientsSurgical resectionCortical hyperexcitabilityUncontrolled seizuresAggressive featuresSeizure activityEpileptogenic focusCortical irritationRisk factors
2016
Altered cortical beta‐band oscillations reflect motor system degeneration in amyotrophic lateral sclerosis
Proudfoot M, Rohenkohl G, Quinn A, Colclough G, Wuu J, Talbot K, Woolrich M, Benatar M, Nobre A, Turner M. Altered cortical beta‐band oscillations reflect motor system degeneration in amyotrophic lateral sclerosis. Human Brain Mapping 2016, 38: 237-254. PMID: 27623516, PMCID: PMC5215611, DOI: 10.1002/hbm.23357.Peer-Reviewed Original ResearchConceptsPrimary lateral sclerosisAmyotrophic lateral sclerosisSensitive marker of disease activityPLS groupMotor cortex of ALS patientsBeta-band oscillationsMarkers of disease activityDevelopment of overt symptomsHealthy control groupALS spectrumAmyotrophic lateral sclerosis patientsAsymptomatic mutation carriersDiffusion tensor imaging studiesBeta desynchronizationSymptomatic patientsLateral sclerosisDisease activityMutation carriersGene mutationsCortical hyperexcitabilityAsymptomatic carriersSensitive markerNeuroprotective strategiesImaging studiesCortical dysfunction
2012
Understanding the Etiology of Tuberous Sclerosis Complex
Bordey A. Understanding the Etiology of Tuberous Sclerosis Complex. 2012 DOI: 10.21236/ada566455.Peer-Reviewed Original ResearchTuberous sclerosis complexTSC lesionsAnimal modelsDiscrete cortical lesionsGenetic multisystem disorderSevere neurological symptomsTsc1 inactivationCortical hyperexcitabilityNeurological symptomsCortical lesionsPerinatal lifeTSC patientsSeizure generationMultisystem disorderFormation of lesionsSignificant causeLesionsLesion formationEtiologyDisordersNovel technical approachHyperexcitabilityMorbidityPatientsSymptoms
2011
Single-cell Tsc1 knockout during corticogenesis generates tuber-like lesions and reduces seizure threshold in mice
Feliciano DM, Su T, Lopez J, Platel JC, Bordey A. Single-cell Tsc1 knockout during corticogenesis generates tuber-like lesions and reduces seizure threshold in mice. Journal Of Clinical Investigation 2011, 121: 1596-1607. PMID: 21403402, PMCID: PMC3069783, DOI: 10.1172/jci44909.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAstrocytesBase SequenceCell SizeCerebral CortexDisease Models, AnimalDNA PrimersFemaleGene Knockout TechniquesMiceMice, 129 StrainMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsMice, TransgenicPregnancySeizuresTOR Serine-Threonine KinasesTuberous SclerosisTuberous Sclerosis Complex 1 ProteinTumor Suppressor ProteinsConceptsTuberous sclerosis complexSeizure thresholdNeuronal populationsSigns of gliosisLower seizure thresholdContribution of astrocytesDiscrete neuronal populationsAutosomal dominant disorderHeterotopic nodulesCortical hyperexcitabilityCortical tubersCortical lesionsGlial reactivityIntractable seizuresCortical malformationsSoma sizeAnimal modelsTSC1 gene productAffected neuronsDendritic treeGiant cellsUtero electroporationMutant miceLesion formationMammalian target
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