2024
A review on polyamines as promising next-generation neuroprotective and anti-aging therapy
Arthur R, Jamwal S, Kumar P. A review on polyamines as promising next-generation neuroprotective and anti-aging therapy. European Journal Of Pharmacology 2024, 978: 176804. PMID: 38950837, DOI: 10.1016/j.ejphar.2024.176804.Peer-Reviewed Original ResearchCognitive dysfunctionNeurodegenerative disordersRegulation of gene expressionProgressive degeneration of neuronsProgrammed cell deathDegeneration of neuronsSymptomatic therapyPharmacological strategiesAnti-oxidative effectsAnti-aging therapyAverage ageProgressive degenerationNeuroprotective effectsLocomotor abnormalitiesIon channelsCell deathBiochemical activityGene expressionPopulation average ageTherapyMolecular mechanismsDisordersPolyamine supplementationDysfunctionAnti-aging effects
2022
Identifying Disease Signatures in the Spinocerebellar Ataxia Type 1 Mouse Cortex
Luttik K, Olmos V, Owens A, Khan A, Yun J, Driessen T, Lim J. Identifying Disease Signatures in the Spinocerebellar Ataxia Type 1 Mouse Cortex. Cells 2022, 11: 2632. PMID: 36078042, PMCID: PMC9454518, DOI: 10.3390/cells11172632.Peer-Reviewed Original ResearchConceptsSCA1 mouse modelSpinocerebellar ataxia type 1Brain regionsMotor cortexMouse modelPurkinje cellsUnique gene expression changesCranial nerve nucleiBroad brain regionsSpecific neuronal populationsCerebellar Purkinje cellsInferior olive nucleusRegion-specific mechanismsCortical pathologyAtaxin-1Synaptic dysfunctionNerve nucleiSpinocerebellar tractSpinal cordProgressive degenerationTranscriptomic changesNeuronal populationsMouse cortexMutant ataxin-1Type 1
2018
Techniques and outcomes of secondary open repair for chronic dissection after acute repair of type A aortic dissection.
Assi R, Bavaria JE, Desai ND. Techniques and outcomes of secondary open repair for chronic dissection after acute repair of type A aortic dissection. The Journal Of Cardiovascular Surgery 2018, 59: 759-766. PMID: 29943963, DOI: 10.23736/s0021-9509.18.10646-x.Peer-Reviewed Original ResearchConceptsAortic dissectionSecondary open repairThoraco-abdominal aortaDistal false lumenRisk of ruptureAcute TAADChronic dissectionAcceptable morbidityAcute typeAcute repairPrimary tearDistal aortaOpen repairAneurysmal dilatationFalse lumenDistal reoperationExperienced handsIndex operationProgressive degenerationSuccessful repairAortaDissectionHybrid procedureRepairReoperation
2017
Guidelines on experimental methods to assess mitochondrial dysfunction in cellular models of neurodegenerative diseases
Connolly NMC, Theurey P, Adam-Vizi V, Bazan NG, Bernardi P, Bolaños JP, Culmsee C, Dawson VL, Deshmukh M, Duchen MR, Düssmann H, Fiskum G, Galindo MF, Hardingham GE, Hardwick JM, Jekabsons MB, Jonas EA, Jordán J, Lipton SA, Manfredi G, Mattson MP, McLaughlin B, Methner A, Murphy AN, Murphy MP, Nicholls DG, Polster BM, Pozzan T, Rizzuto R, Satrústegui J, Slack RS, Swanson RA, Swerdlow RH, Will Y, Ying Z, Joselin A, Gioran A, Moreira Pinho C, Watters O, Salvucci M, Llorente-Folch I, Park DS, Bano D, Ankarcrona M, Pizzo P, Prehn JHM. Guidelines on experimental methods to assess mitochondrial dysfunction in cellular models of neurodegenerative diseases. Cell Death & Differentiation 2017, 25: 542-572. PMID: 29229998, PMCID: PMC5864235, DOI: 10.1038/s41418-017-0020-4.Peer-Reviewed Original ResearchConceptsNeurodegenerative diseasesMitochondrial dysfunctionCellular modelSpectrum of chronicDeath of neuronsViable therapeutic targetPrimary neuron culturesMost neurodegenerative diseasesMitochondrial bioenergetic dysfunctionProgressive degenerationConsensus articleTherapeutic targetNeuron culturesDysfunctionSuch dysfunctionDiseaseHuntington's diseaseNeurodegenerative disease phenotypesBioenergetic dysfunctionDistinct molecular mechanismsCross-disease analysisDisease phenotypeMitochondrial functionCellular bioenergeticsMolecular mechanisms
2006
Slow progressive degeneration of nigral dopaminergic neurons in postnatal Engrailed mutant mice
Sgadò P, Albéri L, Gherbassi D, Galasso SL, Ramakers GM, Alavian KN, Smidt MP, Dyck RH, Simon HH. Slow progressive degeneration of nigral dopaminergic neurons in postnatal Engrailed mutant mice. Proceedings Of The National Academy Of Sciences Of The United States Of America 2006, 103: 15242-15247. PMID: 17015829, PMCID: PMC1622807, DOI: 10.1073/pnas.0602116103.Peer-Reviewed Original ResearchConceptsDopaminergic neuronsProgressive degenerationParkinson's diseaseMutant miceEngrailed-1Postnatal mutant miceSlow progressive degenerationNigral dopaminergic neuronsMesencephalic dopaminergic neuronsRelease of dopamineKey pathological featureLower body weightMotor deficitsPathological featuresSubstantia nigraCaudate putamenNovel treatmentsBody weightNeurodegenerative disordersHeterozygous nullDiseaseMiceNeuronsMolecular etiologyDependent manner
1983
Scrapie-associated fibrils in Creutzfeldt–Jakob disease
Merz P, Somerville R, Wisniewski H, Manuelidis L, Manuelidis E. Scrapie-associated fibrils in Creutzfeldt–Jakob disease. Nature 1983, 306: 474-476. PMID: 6358899, DOI: 10.1038/306474a0.Peer-Reviewed Original ResearchConceptsScrapie associated fibrilsCreutzfeldt-Jakob diseaseCentral nervous systemTitre of infectivityScrapie of sheepInfected brainPathological responseProgressive degenerationNervous systemSynaptosomal preparationsInfectious agentsBrain fractionsTransmissible encephalopathiesDiseaseHuman casesSpleen extractsAbnormal fibrilsSusceptible hostsScrapieClose associationDifferent tissuesEncephalopathyAgentsDegenerationTitres
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply