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000162850 0247_ $$2doi$$a10.1007/s00401-021-02348-6
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000162850 037__ $$aDZNE-2021-01505
000162850 041__ $$aEnglish
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000162850 1001_ $$aZimmer, Till S$$b0
000162850 245__ $$aSeizure-mediated iron accumulation and dysregulated iron metabolism after status epilepticus and in temporal lobe epilepsy.
000162850 260__ $$aHeidelberg$$bSpringer$$c2021
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000162850 520__ $$aNeuronal dysfunction due to iron accumulation in conjunction with reactive oxygen species (ROS) could represent an important, yet underappreciated, component of the epileptogenic process. However, to date, alterations in iron metabolism in the epileptogenic brain have not been addressed in detail. Iron-related neuropathology and antioxidant metabolic processes were investigated in resected brain tissue from patients with temporal lobe epilepsy and hippocampal sclerosis (TLE-HS), post-mortem brain tissue from patients who died after status epilepticus (SE) as well as brain tissue from the electrically induced SE rat model of TLE. Magnetic susceptibility of the presumed seizure-onset zone from three patients with focal epilepsy was compared during and after seizure activity. Finally, the cellular effects of iron overload were studied in vitro using an acute mouse hippocampal slice preparation and cultured human fetal astrocytes. While iron-accumulating neurons had a pyknotic morphology, astrocytes appeared to acquire iron-sequestrating capacity as indicated by prominent ferritin expression and iron retention in the hippocampus of patients with SE or TLE. Interictal to postictal comparison revealed increased magnetic susceptibility in the seizure-onset zone of epilepsy patients. Post-SE rats had consistently higher hippocampal iron levels during the acute and chronic phase (when spontaneous recurrent seizures are evident). In vitro, in acute slices that were exposed to iron, neurons readily took up iron, which was exacerbated by induced epileptiform activity. Human astrocyte cultures challenged with iron and ROS increased their antioxidant and iron-binding capacity, but simultaneously developed a pro-inflammatory phenotype upon chronic exposure. These data suggest that seizure-mediated, chronic neuronal iron uptake might play a role in neuronal dysfunction/loss in TLE-HS. On the other hand, astrocytes sequester iron, specifically in chronic epilepsy. This function might transform astrocytes into a highly resistant, pro-inflammatory phenotype potentially contributing to pro-epileptogenic inflammatory processes.
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000162850 650_7 $$2Other$$aAstrocytes
000162850 650_7 $$2Other$$aGlutathione metabolism
000162850 650_7 $$2Other$$aIron
000162850 650_7 $$2Other$$aStatus epilepticus
000162850 650_7 $$2Other$$aTemporal lobe epilepsy with hippocampal sclerosis
000162850 650_2 $$2MeSH$$aAdult
000162850 650_2 $$2MeSH$$aAged
000162850 650_2 $$2MeSH$$aAged, 80 and over
000162850 650_2 $$2MeSH$$aAnimals
000162850 650_2 $$2MeSH$$aAstrocytes: metabolism
000162850 650_2 $$2MeSH$$aAstrocytes: pathology
000162850 650_2 $$2MeSH$$aCase-Control Studies
000162850 650_2 $$2MeSH$$aCell Culture Techniques
000162850 650_2 $$2MeSH$$aDisease Models, Animal
000162850 650_2 $$2MeSH$$aEpilepsy, Temporal Lobe: complications
000162850 650_2 $$2MeSH$$aEpilepsy, Temporal Lobe: metabolism
000162850 650_2 $$2MeSH$$aEpilepsy, Temporal Lobe: pathology
000162850 650_2 $$2MeSH$$aFemale
000162850 650_2 $$2MeSH$$aHippocampus: metabolism
000162850 650_2 $$2MeSH$$aHumans
000162850 650_2 $$2MeSH$$aIron: metabolism
000162850 650_2 $$2MeSH$$aIron Metabolism Disorders: etiology
000162850 650_2 $$2MeSH$$aIron Metabolism Disorders: pathology
000162850 650_2 $$2MeSH$$aMale
000162850 650_2 $$2MeSH$$aMiddle Aged
000162850 650_2 $$2MeSH$$aOxidative Stress: physiology
000162850 650_2 $$2MeSH$$aRats
000162850 650_2 $$2MeSH$$aStatus Epilepticus: complications
000162850 650_2 $$2MeSH$$aStatus Epilepticus: metabolism
000162850 650_2 $$2MeSH$$aStatus Epilepticus: pathology
000162850 7001_ $$0P:(DE-HGF)0$$aDavid, Bastian$$b1
000162850 7001_ $$aBroekaart, Diede W M$$b2
000162850 7001_ $$0P:(DE-2719)9001203$$aSchidlowski, Martin$$b3$$udzne
000162850 7001_ $$aRuffolo, Gabriele$$b4
000162850 7001_ $$aKorotkov, Anatoly$$b5
000162850 7001_ $$avan der Wel, Nicole N$$b6
000162850 7001_ $$avan Rijen, Peter C$$b7
000162850 7001_ $$aMühlebner, Angelika$$b8
000162850 7001_ $$avan Hecke, Wim$$b9
000162850 7001_ $$aBaayen, Johannes C$$b10
000162850 7001_ $$aIdema, Sander$$b11
000162850 7001_ $$aFrançois, Liesbeth$$b12
000162850 7001_ $$avan Eyll, Jonathan$$b13
000162850 7001_ $$aDedeurwaerdere, Stefanie$$b14
000162850 7001_ $$aKessels, Helmut W$$b15
000162850 7001_ $$aSurges, Rainer$$b16
000162850 7001_ $$aRüber, Theodor$$b17
000162850 7001_ $$aGorter, Jan A$$b18
000162850 7001_ $$aMills, James D$$b19
000162850 7001_ $$avan Vliet, Erwin A$$b20
000162850 7001_ $$00000-0002-3542-3770$$aAronica, Eleonora$$b21
000162850 773__ $$0PERI:(DE-600)1458410-4$$a10.1007/s00401-021-02348-6$$gVol. 142, no. 4, p. 729 - 759$$n4$$p729 - 759$$tActa neuropathologica$$v142$$x1432-0533$$y2021
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