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Cher Bachar
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Neurological and Psychiatric disorders Mindmap am Demyelinating disorders, erstellt von Cher Bachar am 24/05/2013.

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Cher Bachar
Erstellt von Cher Bachar vor mehr als 11 Jahre
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Demyelinating disordersClassificationMultiple sclerosis(MS)post infeciousencephalomyelitisprogressive multifocalleucoencephalophytoxic and nutritionaldisordersleucodystrophiesDisorders affecting solely orpredominately the peripheral nervoussystemMultiple sclerosis (MS)Etiology andincidenceonset- 20-45yrwomen are more affectedcause?immunological abnormalitiesgenetic suseptibilitylow sun levels- more riskautoimmune attackT-cellsMacrophagessecret inflammatorycytokines and chemikinesresults in demyelination andimpairement in signal coductionstrip myelinStage 1- inflammatory phaseStage 2- degenerative phaseT cells, macrophages-cytokines, chemokinesT-cells- excessglutamate releaseremyelination failure- recoveryrequires a sequence ofsteps- cell interactionClinical featuresMechanismsDiagnosisMRI imagingoligoclonal presence inCSF and serumOligoclonal band testCNS lesions- disseminatedin more than one areaManagementmuscle trainingplagues or islands of demyelinationprimarily in white matterperiventricular regionsoptic nervesspinal cordsubcortical white mattercerebral cortex (mostcases)brainstemcerebellumTypes95% have IgG in the CSFisoelectric focusing using agarose gelsS-ve, C-ve= normalS-ve, C+ve= MSS+ve, C+ve= Guillain-Barre syndromeS+ve, C+ve= viral encephalitissymptomsremitting relapsingsecondary progressivePrimary progressive (<15%)Progressive relapsing (<5%)completepartialrelapsesno relapsesAcute- supression of inflammationminimizing handicapReduce relapse + suppress ongoing disease activityControl muscle tonedrugscorticosteriodsinterferon-B, glatiramer acetate, natalizumabhistory of relapsesand remissionsBlood testsPeriventricular leukomalacia (PVL)loss of myelinating oligodendrocytes(OLs) and OL progenitor cells (OPCs)Oxidative damageExcitotoxicityPro-inflammatory cytokinesGenetic alterationsOPCexpress NG2 and PDGFαRmyelin production-energy-ATP-dependentbyproduct- hydrogen peroxidecause DNA degradation and OL apoptosisperoxisomes- present in OLbyproduct- hydrogen peroxideCellular metabolismmyelin syntheticenzymes require ironfree radical formationSphingolipids - apoptosiscontain Deathreceptors (DRs)apoptotic cascadesceramide - second messengeractivates DRs- OL apoptosisamyloid-β peptideelevated gluatamteOLs / immature OLsCNS pathalogymacrophages and microglia>> prolonged activation of receptorshigh Ca levelsactivating enzymesthat degradecytoskeletal proteinscausing mitochondrial disruption leadingto reactive oxygen species productionstudies- OLs and myelin arevulnerable to Glu excitotoxicityAMPAR/ NMDAR present in OLsevidenceAMPAR vs NMDARcytokines IL-1β, IL-2,interferon γ (IFNγ), and TNFαdirect and/or indirectTNFα - p55 TNF receptorTNFα - microglial andmacrophage activationactivate SMase-leading to ceramideup-regulate the transcription factor p53cell death receptorsirradiation-induced OL deathAlexander’s diseasemutations in the astrocyte glial fibrillaryacidic protein (GFAP) geneAdrenoleukodystrophydefect in the ABCD1 geneNeurodegenerationtransition into the progressivedisease phase - critical loss ofaxon densityMRI, MRS, pathological studiesHypothesisinflammation-related mechanisms mightover time initiate an autonomousneurodegenerative processthat (adaptive or innate) immunemechanisms in the nonlesional whitematter might substantially contribute tothe extent of neuroaxonal damagethat Wallerian and retrograde degeneration initiatedby axonal transections in focally demyelinatedlesions may explain the wealth of neuroaxonal lossobservedalternative hypothesis considers MS as a primarydegenerative disease in individuals in whom certainfeatures of their immune system favor a very strong,albeit secondary, immune responseearly stagespathological substrate(s) of theprogressive disease phaseNeuroaxonal dysfunction or demisemeningeal inflammationcorrelated with neuronal/ axonal lossongoing adaptive immune cellinfiltration correlated with APPT-cells- induceneuronal damageenhanced microglia activationinflammatory response in nonlesioned tissues,and upregulated inflammatory pathwaysneuroaxonal cytoskeletonDoppelklick auf diesen KnotenKlicke und ziehe diese Schaltfläche, um einen neuen Knoten zu erstellen