Evidence map›Paper›PMID 35317335›Full record

ArticleWorld journal of psychiatry2022

Reduced paraoxonase 1 activities may explain the comorbidities between temporal lobe epilepsy and depression, anxiety and psychosis.

Ana Paula Michelin, Michael H J Maes, Thitiporn Supasitthumrong, Chusak Limotai, Andressa Keiko Matsumoto, Laura de Oliveira Semeão, João Victor de Lima Pedrão, Estefânia Gastaldello Moreira, Buranee Kanchanatawan, Décio Sabbatini Barbosa

Open access · diamondAbstract read
In one paragraph

Article in World journal of psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Ana Paula MichelinHealth Sciences Center, State University of Londrina, Londrina 86038-440, Brazil.
Michael H J MaesDepartment of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
Thitiporn SupasitthumrongDepartment of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
Chusak LimotaiChulalongkorn Comprehensive Epilepsy Center of Excellence, King Chulalongkorn Memorial Hospital, The Thai Red Cross Society, Bangkok 10330, Thailand.
Andressa Keiko MatsumotoHealth Sciences Center, State University of Londrina, Londrina 86038-440, Brazil.
Laura de Oliveira SemeãoHealth Sciences Center, State University of Londrina, Londrina 86038-440, Brazil.
João Victor de Lima PedrãoHealth Sciences Center, State University of Londrina, Londrina 86038-440, Brazil.
Estefânia Gastaldello MoreiraHealth Sciences Center, State University of Londrina, Londrina 86038-440, Brazil.
Buranee KanchanatawanDepartment of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
Décio Sabbatini BarbosaHealth Sciences Center, State University of Londrina, Londrina 86038-440, Brazil.
Chulalongkorn University · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTemporal lobe epilepsy (TLE) is the most common focal epilepsy subtype in adults and is frequently accompanied by depression, anxiety and psychosis. Aberrations in total paraoxonase 1 (PON1) status may occur in TLE and these psychiatric conditions.

aimTo examine PON1 status, namely Q192R PON1 genotypes and PON1 enzymatic activities, in TLE.

methodsWe recruited 40 normal controls and 104 TLE patients, 27 without comorbidities and 77 with comorbidities including mood disorders (

resultsFour-(chloromethyl)phenyl acetate hydrolysis (CMPAase) and arylesterase activities were significantly lower in TLE and mesial temporal sclerosis (MTS) with and without psychiatric comorbidities than those in normal controls. The areas under the receiver operating characteristic curve of CMPAase were 0.893 (0.037) for TLE and 0.895 (± 0.037) for MTS. Partial least squares path analysis showed that there were specific indirect effects of PON1 genotype on TLE severity (

conclusionThe severity of TLE and comorbidities are to a large extent explained by reduced PON1 enzyme activities and by effects of the Q192R genotype, which are mediated by reduced CMPAase activity. Total PON1 status plays a key role in the pathophysiology of TLE, MTS and psychiatric comorbidities by increasing the risk of oxidative toxicity. PON1 enzyme activities are new drug targets in TLE to treat seizure frequency and psychiatric comorbidities.

Indexed as

Affective disordersAntioxidantsMajor depressionMood disordersNeuroimmuneOxidative stress

Identifiers

PMID35317335
PMCPMC8900591
OpenAlexW4221013213

What Socratic holds

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LicenceCC BY-NC
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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 Socratic graph.