Evidence map›Paper›PMID 36622561›Full record

ArticleMolecular neurobiology2023

Hyperphosphorylated Tau in Mesial Temporal Lobe Epilepsy: a Neuropathological and Cognitive Study.

Eliana C B Toscano, Érica L M Vieira, Lea T Grinberg, Natalia P Rocha, Joseane A S Brant, Regina S Paradela, Alexandre V Giannetti, Claudia K Suemoto, Renata E P Leite, Ricardo Nitrini and 2 more

Open access · greenAbstract read
In one paragraph

Article in Molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
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  12. Exploring biomarkers of neurodegeneration in epilepsy: Critical insights.Epileptic disorders : international epilepsy journal with videotape · 2025
    Review
  13. Hyperphosphorylated Tau and Cognition in Epilepsy.Journal of clinical medicine · 2025
    Review
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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 6 institutions in 3 countries.

Eliana C B ToscanoDepartamento de Patologia Geral, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil. elianacbtoscano@gmail.com.ORCID http://orcid.org/0000-0002-8756-0689
Érica L M VieiraCentre for Addiction and Mental Healthy (CAMH), Toronto, ON, Canada.
Lea T GrinbergBiobank for Aging Studies, Universidade de São Paulo, São Paulo, SP, Brazil.
Natalia P RochaThe Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, USA.
Joseane A S BrantDepartamento de Neurocirurgia, Hospital das Clínicas da Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
Regina S ParadelaBiobank for Aging Studies, Universidade de São Paulo, São Paulo, SP, Brazil.
Alexandre V GiannettiDepartamento de Neurocirurgia, Hospital das Clínicas da Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
Claudia K SuemotoBiobank for Aging Studies, Universidade de São Paulo, São Paulo, SP, Brazil.
Renata E P LeiteBiobank for Aging Studies, Universidade de São Paulo, São Paulo, SP, Brazil.
Ricardo NitriniBiobank for Aging Studies, Universidade de São Paulo, São Paulo, SP, Brazil.
Milene A RachidDepartamento de Patologia Geral, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
Antonio L TeixeiraFaculdade Santa Casa BH, Belo Horizonte, Brazil; Neuropsychiatry Program, Department of Psychiatry and Behavioral Sciences, The University of Texas Health Science Center at Houston, Houston, TX, USA.
Universidade de São Paulo · BRHospital das Clínicas da Universidade Federal de Minas Gerais · BRThe University of Texas Health Science Center at Houston · USCentre for Addiction and Mental Health · CAUniversidade Federal de Juiz de Fora · BRUniversidade Federal de Minas Gerais · BR

Funding

Clinical Features and Neuropathological Basis of Sleep Wake Behavior in Alzheimer's and PSPR01AG060477 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Lea Tenenholz Grinberg, Thomas C Neylan · 2019 to 2026
$8.2M
Neuropathological changes underlying clinical heterogeneity in Alzheimer diseaseK24AG053435 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GRINBERG, LEA TENENHOLZ · 2016 to 2025
$1.8M
NIA NIH HHS K24 AG053435NIA NIH HHS R01 AG060477
6 · The paper itself

Abstract

Temporal lobe epilepsy (TLE) often courses with cognitive deficits, but its underlying neuronal basis remains unclear. Confluent data suggest that epilepsy share pathophysiological mechanisms with neurodegenerative diseases. However, as most studies analyze subjects 60 years old and older, it is challenging to rule out that neurodegenerative changes arise from age-related mechanisms rather than epilepsy in these individuals. To fill this gap, we conducted a neuropathological investigation of the hippocampal formation of 22 adults with mesial TLE and 20 age- and sex-matched controls (both younger than 60 years). Moreover, we interrogated the relationship between these neuropathological metrics and cognitive performance. Hippocampal formation extracted from patients with drug-resistant mesial TLE undergoing surgery and postmortem non-sclerotic hippocampal formation of clinically and neuropathologically controls underwent immunohistochemistry against amyloid β (Aβ), hyperphosphorylated tau (p-tau), and TAR DNA-binding protein-43 (TDP-43) proteins, followed by quantitative analysis. Patients underwent a comprehensive neuropsychological evaluation prior to surgery. TLE hippocampi showed a significantly higher burden of p-tau than controls, whereas Aβ deposits and abnormal inclusions of TDP-43 were absent in both groups. Patients with hippocampal sclerosis (HS) type 2 had higher immunostaining for p-tau than patients with HS type 1. In addition, p-tau burden was associated with impairment in attention tasks and seizures frequency. In this series of adults younger than 60 years-old, the increase of p-tau burden associated with higher frequency of seizures and attention impairment suggests the involvement of tau pathology as a potential contributor to cognitive deficits in mesial TLE.

Indexed as

Drug Resistant EpilepsyEpilepsy, Temporal LobeAdultAmyloid beta-PeptidesCognitionHippocampusHumansMiddle AgedSeizuresAmyloid beta-PeptidesCognitionDrug-resistant epilepsyNeurodegenerationp-tau

Identifiers

PMID36622561
PMCPMC10084588
OpenAlexW4313829367

What OpenQuestion holds

Textmetadata
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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.