2023
Regional Homogeneity in schizophrenia patients with tardive dyskinesia: a resting-state fMRI study
Yu T, Li Y, Li N, Huang J, Fan F, Luo X, Tan S, Yang F, Tian B, Tian L, Li C, Tan Y. Regional Homogeneity in schizophrenia patients with tardive dyskinesia: a resting-state fMRI study. Psychiatry Research Neuroimaging 2023, 335: 111724. PMID: 37871408, DOI: 10.1016/j.pscychresns.2023.111724.Peer-Reviewed Original ResearchConceptsAbnormal Involuntary Movement ScaleTardive dyskinesiaInferior semilunar lobuleSchizophrenia patientsCourse of TDRegional homogeneityResting-state functional magnetic resonance imagingResting-state fMRI studySeverity of TDCerebral regional homogeneityUpper limb scoreNegative Syndrome ScaleNon-TD groupMedial frontal gyrusFunctional magnetic resonance imagingMagnetic resonance imagingLower ReHoReHo valuesHigher ReHoLimb scoreNeuronal degenerationHealthy controlsFunctional abnormalitiesMovement ScaleLeft supramarginal gyrusMicrobiota and Diapause-Induced Neuroprotection Share a Dependency on Calcium But Differ in Their Effects on Mitochondrial Morphology
Delgado S, Urrutia A, Gutzwiller F, Chiu C, Calixto A. Microbiota and Diapause-Induced Neuroprotection Share a Dependency on Calcium But Differ in Their Effects on Mitochondrial Morphology. ENeuro 2023, 10: eneuro.0424-22.2023. PMID: 37385728, PMCID: PMC10368204, DOI: 10.1523/eneuro.0424-22.2023.Peer-Reviewed Original ResearchConceptsCaenorhabditis elegans</i>Length of mitochondriaDiapause entryLactate-producing bacteriaReverse geneticsGut microbiotaMitochondrial morphologyTranscriptomic approachMitochondrial sizeMitochondrial functionMicrobiotaMechanistic commonalitiesEnvironmental variablesBacteriaMCU-1GenesNeuronal functionMultiple mechanismsCalcium homeostasisDiapauseNeuronal degenerationNeuronal protectionRegeneration of damaged neuronsFood deprivationTranscriptome
2020
Fronto-temporal dementia risk gene TMEM106B has opposing effects in different lysosomal storage disorders
Perez-Canamas A, Takahashi H, Lindborg JA, Strittmatter SM. Fronto-temporal dementia risk gene TMEM106B has opposing effects in different lysosomal storage disorders. Brain Communications 2020, 3: fcaa200. PMID: 33796852, PMCID: PMC7990118, DOI: 10.1093/braincomms/fcaa200.Peer-Reviewed Original ResearchNeuronal ceroid lipofuscinosisLysosomal compartmentGenome-wide association studiesCeroid lipofuscinosisGaucher diseaseLysosomal storage disorderEndo-lysosomal compartmentsTransmembrane proteinStorage disorderVacuolar ATPaseNull phenotypeATPase stateFrontotemporal lobar degenerationAssociation studiesConduritol B epoxidePurkinje cell degenerationLysosomal acidificationMouse phenotypeNeurodegenerative lysosomal diseaseDifferent lysosomal storage disordersTMEM106BNeuronal lossMotor deficitsNeuronal degenerationPhenotype
2016
TREM2-mediated early microglial response limits diffusion and toxicity of amyloid plaques
Wang Y, Ulland TK, Ulrich JD, Song W, Tzaferis JA, Hole JT, Yuan P, Mahan TE, Shi Y, Gilfillan S, Cella M, Grutzendler J, DeMattos RB, Cirrito JR, Holtzman DM, Colonna M. TREM2-mediated early microglial response limits diffusion and toxicity of amyloid plaques. Journal Of Experimental Medicine 2016, 213: 667-675. PMID: 27091843, PMCID: PMC4854736, DOI: 10.1084/jem.20151948.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseTREM2 deficiencyAβ accumulationNeuritic damageAβ plaquesMyeloid cellsAbsence of TREM2Impact of TREM2Rare TREM2 variantsAmyloid β accumulationBrain-resident microgliaMyeloid cells 2Peripheral blood monocytesEarly time pointsMicroglial clusteringMicroglial receptorΒ accumulationAβ depositsNeuronal degenerationTREM2 variantsAmyloid plaquesMurine modelBlood monocytesMatter of debateMicroglia
2015
Mice lacking glutamate carboxypeptidase II develop normally, but are less susceptible to traumatic brain injury
Gao Y, Xu S, Cui Z, Zhang M, Lin Y, Cai L, Wang Z, Luo X, Zheng Y, Wang Y, Luo Q, Jiang J, Neale JH, Zhong C. Mice lacking glutamate carboxypeptidase II develop normally, but are less susceptible to traumatic brain injury. Journal Of Neurochemistry 2015, 134: 340-353. PMID: 25872793, DOI: 10.1111/jnc.13123.Peer-Reviewed Original ResearchConceptsTraumatic brain injuryGlutamate carboxypeptidase IIModerate traumatic brain injuryNeurotransmitter N-acetylaspartylglutamateGCPII geneBrain injuryNervous systemSpatial learning/memoryEnhanced glutamate transmissionLong-term behavioral outcomesHippocampus 24 hInhibition of GCPIIWild-type littermatesMorris water mazeCarboxypeptidase IIKO mouse lineLearning/memoryHistopathological protectionGene KOBeam walkingGlutamate transmissionNeuronal degenerationAstrocyte damageKO miceNeurological behavior
2013
Rapid and Permanent Neuronal Inactivation In Vivo via Subcellular Generation of Reactive Oxygen with the Use of KillerRed
Williams DC, Bejjani RE, Ramirez PM, Coakley S, Kim SA, Lee H, Wen Q, Samuel A, Lu H, Hilliard MA, Hammarlund M. Rapid and Permanent Neuronal Inactivation In Vivo via Subcellular Generation of Reactive Oxygen with the Use of KillerRed. Cell Reports 2013, 5: 553-563. PMID: 24209746, PMCID: PMC3877846, DOI: 10.1016/j.celrep.2013.09.023.Peer-Reviewed Original ResearchConceptsReactive oxygen speciesC. elegansGenetic toolsOrganelle fragmentationPlasma membraneSpecific developmental outcomesSubcellular responsesCell deathKillerRedReactive oxygenOxygen speciesTargeted cellCircuit functionSingle light stimulusSingle animalInactivationElegansCellsVivoCell bodiesSpeciesNeuronal degenerationNeuronsAnimalsNeuronal inactivation
2010
Estrogen Promotes Parvalbumin Expression in Arcuate Nucleus POMC Neurons
Sotonyi P, Gao Q, Bechmann I, Horvath TL. Estrogen Promotes Parvalbumin Expression in Arcuate Nucleus POMC Neurons. Reproductive Sciences 2010, 17: 1077-1080. PMID: 20713969, DOI: 10.1177/1933719110379651.Peer-Reviewed Original ResearchConceptsPOMC neuronsArcuate nucleus neuronsLean body massSuppression of feedingSuppress appetiteParvalbumin expressionEstrogen treatmentHypothalamic neuronsArcuate nucleusNeuronal degenerationNucleus neuronsFemale miceCalcium overloadExcitatory activityCalcium-binding proteinsCalcium influxReceptor presenceCalcium entrySustained satietyNeuronsEnergy expenditureEstradiolParvalbuminAppetiteBody mass
2003
Mitochondrial Uncoupling Proteins: Regulators of Retinal Cell Death
Barnstable CJ, Li M, Reddy R, Horvath TL. Mitochondrial Uncoupling Proteins: Regulators of Retinal Cell Death. Advances In Experimental Medicine And Biology 2003, 533: 269-275. PMID: 15180273, DOI: 10.1007/978-1-4615-0067-4_33.Peer-Reviewed Original ResearchConceptsOxidative stressElevated levelsOptic nerve disordersGanglion cell deathCell deathRetinal cell deathSuch elevated levelsNerve disordersInner retinaNeuronal degenerationReactive oxygen radicalsMetabolic conditionsNeural componentsApoptotic cell deathOxygen radicalsIntracellular metabolismDeathSpecific mutationsCell typesExtensive evidenceIrreversible cascadeGlaucomaDegenerationRetina
2002
Nicotinic receptors in aging and dementia
Picciotto MR, Zoli M. Nicotinic receptors in aging and dementia. Developmental Neurobiology 2002, 53: 641-655. PMID: 12436427, DOI: 10.1002/neu.10102.Peer-Reviewed Original ResearchConceptsNicotinic agonistsCognitive functionNeuronal nicotinic acetylcholine receptorsDevelopment of dementiaNicotinic acetylcholine receptorsCholinergic markersCholinergic functionNeuronal degenerationNicotinic receptorsEpidemiological studiesNicotinic functionAnimal studiesNeurodegenerative illnessesAcetylcholine receptorsCognitive deficitsDementiaNeurodegenerative diseasesImpaired subjectsDistinct actionsPatientsAgonistsDiseaseNicotineReceptorsSmoking
1999
Ratio of S-nitrosohomocyst(e)ine to homocyst(e)ine or other thiols determines neurotoxicity in rat cerebrocortical cultures
D'Emilia D, Lipton S. Ratio of S-nitrosohomocyst(e)ine to homocyst(e)ine or other thiols determines neurotoxicity in rat cerebrocortical cultures. Neuroscience Letters 1999, 265: 103-106. PMID: 10327179, DOI: 10.1016/s0304-3940(99)00210-4.Peer-Reviewed Original ResearchConceptsN-methyl-D-aspartate agonistRat cerebrocortical culturesS-nitrosocysteineS-nitrosohomocysteineNeuronal degenerationCerebrocortical culturesS-nitrosothiolsSubsequent neurotoxicityAcute exposureDetermine outcomeNitric oxideForm peroxynitriteNeurotoxicityS-nitrosylationEndogenous O2S-nitrosoproteinsAgonists
1998
Tracing of the entorhinal‐hippocampal pathway in vitro
Kluge A, Hailer N, Horvath T, Bechmann I, Nitsch R. Tracing of the entorhinal‐hippocampal pathway in vitro. Hippocampus 1998, 8: 57-68. PMID: 9519887, DOI: 10.1002/(sici)1098-1063(1998)8:1<57::aid-hipo6>3.0.co;2-4.Peer-Reviewed Original ResearchConceptsOuter molecular layerPerforant pathDentate gyrusEntorhinal cortexEntorhinal-hippocampal interactionPerforant path axonsOrganotypic slice culturesMini-RubyPerforant fibersVitro tracingAnterograde degenerationDendritic shaftsLesion paradigmMicroglial cellsNeuronal degenerationEntorhinal neuronsNeurotoxin treatmentMolecular layerSlice culturesAxonal materialGrowth factorSubsequent phagocytosisGyrusEntorhinal-hippocampal regionFurther studies
1993
The Therapeutic Potential of Neurotrophic Factors in the Treatment of Parkinson's Disease
Lindsay R, Altar C, Cedarbaum J, Hyman C, Wiegand S. The Therapeutic Potential of Neurotrophic Factors in the Treatment of Parkinson's Disease. Experimental Neurology 1993, 124: 103-118. PMID: 8282068, DOI: 10.1006/exnr.1993.1181.Peer-Reviewed Original ResearchConceptsNeurotrophic factorParkinson's diseaseNeurodegenerative disordersTherapeutic agentsNeurodegenerative diseasesFetal nigral graftsTransplantation of neuronsDopamine neurotrophic factorPartial symptomatic reliefDopamine receptor agonistsNeurotrophic growth factorsPotential clinical useHuman neurodegenerative disordersAppropriate neurotransmittersObvious therapeutic strategyNeuronal lossNigral graftsSymptomatic reliefDevelopment of drugsDopaminergic neuronsNeuroprotective agentsSubstantia nigraNeuronal degenerationNeurotrophin familyDopamine neuronsMolecular mechanisms of trauma-induced neuronal degeneration.
Lipton S. Molecular mechanisms of trauma-induced neuronal degeneration. Current Opinion In Neurology 1993, 6: 588-96. PMID: 8400474.Peer-Reviewed Original Research
1991
Fetal akinesia deformation sequence (Pena-Shokeir phenotype) associated with acquired intrauterine brain damage.
Lavi E, Montone K, Rorke L, Kliman H. Fetal akinesia deformation sequence (Pena-Shokeir phenotype) associated with acquired intrauterine brain damage. Neurology 1991, 41: 1467-8. PMID: 1891100, DOI: 10.1212/wnl.41.9.1467.Peer-Reviewed Original ResearchConceptsIntrauterine brain damageFocal cerebral infarctionTetralogy of FallotFetal akinesia deformation sequenceCocaine-using mothersPena-Shokeir phenotypeDiffuse brainstemCerebral infarctionNeuropathologic findingsPulmonary hypoplasiaIschemic damagePathologic findingsNeuronal degenerationBrain damageFacial anomaliesFallotInfarctionBrainstemTetralogyInfantsHypoplasiaCamptodactylyArthrogryposisFindingsDegeneration
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