Evidence map›Paper›PMID 31869431›Full record

ArticleNeuropathology and applied neurobiology2020

Chronic activation of anti-oxidant pathways and iron accumulation in epileptogenic malformations.

T S Zimmer, G Ciriminna, A Arena, J J Anink, A Korotkov, F E Jansen, W van Hecke, W G Spliet, P C van Rijen, J C Baayen and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Neuropathology and applied neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 3 countries.

T S ZimmerDepartment of (Neuro)Pathology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, The Netherlands.ORCID 0000-0002-6869-3697
G CiriminnaDepartment of (Neuro)Pathology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, The Netherlands.ORCID 0000-0003-4896-803X
A ArenaDepartment of (Neuro)Pathology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, The Netherlands.
J J AninkDepartment of (Neuro)Pathology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, The Netherlands.
A KorotkovDepartment of (Neuro)Pathology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, The Netherlands.
F E JansenDepartment of Paediatric Neurology, University Medical Center Utrecht, The Netherlands.
W van HeckeDepartment of Pathology, University Medical Center Utrecht, The Netherlands.
W G SplietDepartment of Pathology, University Medical Center Utrecht, The Netherlands.
P C van RijenDepartment of Neurosurgery, Brain Centre, Rudolf Magnus Institute for Neuroscience, University Medical Center Utrecht, Utrecht, The Netherlands.
J C BaayenDepartment of Neurosurgery, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam, The Netherlands.
S IdemaDepartment of Neurosurgery, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam, The Netherlands.
N R RensingDepartment of Neurology, Washington University, Saint Louis, MO, USA.
M WongDepartment of Neurology, Washington University, Saint Louis, MO, USA.
J D MillsDepartment of (Neuro)Pathology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, The Netherlands.
E A van VlietDepartment of (Neuro)Pathology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, The Netherlands.ORCID 0000-0001-5747-3202
E AronicaDepartment of (Neuro)Pathology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, The Netherlands.
Amsterdam Neuroscience · NLUniversity Medical Center Utrecht · NLWashington University in St. Louis · USNetherlands Institute for Neuroscience · NL

Funding

MECHANISMS OF BRAIN DYSFUNCTION IN TUBEROUS SCLEROSISR01NS056872 · NINDS · WASHINGTON UNIVERSITY · PI WONG, MICHAEL · 2006 to 2019
$4.0M
NINDS NIH HHS R01 NS056872
6 · The paper itself

Abstract

aimsOxidative stress is evident in resected epileptogenic brain tissue of patients with developmental brain malformations related to mammalian target of rapamycin activation: tuberous sclerosis complex (TSC) and focal cortical dysplasia type IIb (FCD IIb). Whether chronic activation of anti-oxidant pathways is beneficial or contributes to pathology is not clear.

methodsWe investigated oxidative stress markers, including haem oxygenase 1, ferritin and the inflammation associated microRNA-155 in surgically resected epileptogenic brain tissue of TSC (n = 10) and FCD IIb (n = 8) patients and in a TSC model (Tsc1

resultsResected TSC or FCD IIb tissue displayed higher expression of oxidative stress markers and microRNA-155. Tsc1

conclusionOur results demonstrate that early and sustained activation of anti-oxidant signalling and dysregulation of iron metabolism are a pathological hallmark of FCD IIb and TSC. Our findings suggest novel therapeutic strategies aimed at controlling the pathological link between both processes.

Indexed as

Metabolic Networks and PathwaysAnimalsAntioxidantsCells, CulturedEncephalitisEpilepsyFemaleFerritinsGlial Fibrillary Acidic ProteinHeme Oxygenase-1HumansIronMaleMalformations of Cortical DevelopmentMalformations of Cortical Development, Group IMiceAntioxidantsFerritinsGlial Fibrillary Acidic Proteinglial fibrillary astrocytic protein, mouseHeme Oxygenase-1IronMicroRNAsMirn155 microRNA, mouseepilepsyfocal cortical dysplasiahaem oxygenase 1iron metabolismoxidative stresstuberous sclerosis complex

Identifiers

PMID31869431
PMCPMC7308211
OpenAlexW2997791853

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.