Evidence map›Paper›PMID 30539418›Full record

ArticleCellular and molecular neurobiology2019

ATP Synthase Subunit Beta Immunostaining is Reduced in the Sclerotic Hippocampus of Epilepsy Patients.

Marcelo Vilas Boas Mota, Bruna Cunha Zaidan, Amanda Morato do Canto, Enrico Ghizoni, Helder Tedeschi, Luciano de Souza Queiroz, Marina K M Alvim, Fernando Cendes, Iscia Lopes-Cendes, André Almeida Schenka and 2 more

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Benchmarking the proteomic profile of animal models of mesial temporal epilepsy.Annals of clinical and translational neurology · 2022
    Article
  4. Article
  5. Article
  6. Neuroproteomics in Epilepsy: What Do We Know so Far?Frontiers in molecular neuroscience · 2020
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

Marcelo Vilas Boas MotaDepartment of Anatomical Pathology, School of Medical Sciences, University of Campinas (UNICAMP), Av. Tessália Vieira de Camargo, 126, Campinas, SP, CEP 13083-887, Brazil.
Bruna Cunha ZaidanDepartment of Anatomical Pathology, School of Medical Sciences, University of Campinas (UNICAMP), Av. Tessália Vieira de Camargo, 126, Campinas, SP, CEP 13083-887, Brazil.
Amanda Morato do CantoDepartment of Medical Genetics, School of Medical Sciences, University of Campinas (UNICAMP), Av. Tessália Vieira de Camargo, 126, Campinas, SP, CEP 13083-887, Brazil.
Enrico GhizoniDepartment of Neurology, School of Medical Sciences, University of Campinas (UNICAMP), Av. Tessália Vieira de Camargo, 126, Campinas, SP, CEP 13083-887, Brazil.
Helder TedeschiDepartment of Neurology, School of Medical Sciences, University of Campinas (UNICAMP), Av. Tessália Vieira de Camargo, 126, Campinas, SP, CEP 13083-887, Brazil.
Luciano de Souza QueirozDepartment of Anatomical Pathology, School of Medical Sciences, University of Campinas (UNICAMP), Av. Tessália Vieira de Camargo, 126, Campinas, SP, CEP 13083-887, Brazil.
Marina K M AlvimDepartment of Neurology, School of Medical Sciences, University of Campinas (UNICAMP), Av. Tessália Vieira de Camargo, 126, Campinas, SP, CEP 13083-887, Brazil.
Fernando CendesDepartment of Neurology, School of Medical Sciences, University of Campinas (UNICAMP), Av. Tessália Vieira de Camargo, 126, Campinas, SP, CEP 13083-887, Brazil.
Iscia Lopes-CendesDepartment of Medical Genetics, School of Medical Sciences, University of Campinas (UNICAMP), Av. Tessália Vieira de Camargo, 126, Campinas, SP, CEP 13083-887, Brazil.
André Almeida SchenkaDepartment of Pharmacology, School of Medical Sciences, University of Campinas (UNICAMP), Av. Tessália Vieira de Camargo, 126, Campinas, SP, CEP 13083-887, Brazil.
André Schwambach VieiraDepartment of Structural and Functional Biology, Institute of Biology, University of Campinas (UNICAMP), R. Monteiro Lobato, 255, Campinas, SP, CEP 13083-852, Brazil.
Fabio RogerioDepartment of Anatomical Pathology, School of Medical Sciences, University of Campinas (UNICAMP), Av. Tessália Vieira de Camargo, 126, Campinas, SP, CEP 13083-887, Brazil. fabio@fcm.unicamp.br.ORCID http://orcid.org/0000-0001-5712-7617
Universidade Estadual de Campinas (UNICAMP) · BR

Funding

Fundação de Amparo à Pesquisa do Estado de São Paulo (BR) 2013/07559-3
6 · The paper itself

Abstract

Epilepsy is a common disease presenting with recurrent seizures. Hippocampal sclerosis (HS) is the commonest histopathological alteration in patients with temporal lobe epilepsy (TLE) undergoing surgery. HS physiopathogenesis is debatable. We have recently studied, by using mass spectrometry-based proteomics, an experimental model of TLE induced by electrical stimulation. Specifically, protein expressions of both the beta subunit of mitochondrial ATP synthase (ATP5B) and of membrane ATPases were found to be reduced. Here, we investigated tissue distribution of ATP5B and sodium/potassium-transporting ATPase subunit alpha-3 (NKAα3), a protein associated with neuromuscular excitability disorders, in human hippocampi resected "en bloc" for HS treatment (n = 15). We used immunohistochemistry and the stained area was digitally evaluated (increase in binary contrast of microscopic fields) in the hippocampal sectors (CA1-CA4) and dentate gyrus. All HS samples were classified as Type 1, according to the International League Against Epilepsy (ILAE) 2013 Classification (predominant cell loss in CA1 and CA4). ATP5B was significantly decreased in all sectors and dentate gyrus of HS patients compared with individuals submitted to necropsy and without history of neurological alterations (n = 10). NKAα3 expression showed no difference. Moreover, we identified a negative correlation between frequency of pre-operative seizures and number of neurons in CA1. In conclusion, our data showed similarity between changes in protein expression in a model of TLE and individuals with HS. ATP5B reduction would be at least in part due to neuronal loss. Future investigations on ATP5B activity could provide insights into the process of such cell loss.

Indexed as

AdolescentAdultCell CountDentate GyrusEpilepsyFemaleHippocampusHumansImmunohistochemistryMaleMiddle AgedMitochondrial Proton-Translocating ATPasesNeuronsSclerosisSodium-Potassium-Exchanging ATPaseYoung AdultATP5F1B protein, humanMitochondrial Proton-Translocating ATPasesSodium-Potassium-Exchanging ATPaseEpilepsyHippocampal sclerosisImmunohistochemistryMitochondrial ATP synthaseProteomicsSodium/potassium ATPase

Identifiers

PMID30539418
PMCPMC11469864
OpenAlexW2904667596

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.