Evidence map›Paper›PMID 38110905›Full record

ArticleBMC neuroscience2023

Exercise combined with postbiotics treatment results in synergistic improvement of mitochondrial function in the brain of male transgenic mice for Alzheimer's disease.

Attila Kolonics, Zoltán Bori, Ferenc Torma, Dora Abraham, János Fehér, Zsolt Radak

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 17 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

6 authors at 3 institutions in 3 countries.

Attila KolonicsResearch Centre for Molecular Exercise Science, Hungarian University of Sport Science, Alkotas str. 44, Budapest, 1123, Hungary. ka1966a@gmail.com.
Zoltán BoriResearch Centre for Molecular Exercise Science, Hungarian University of Sport Science, Alkotas str. 44, Budapest, 1123, Hungary.
Ferenc TormaResearch Centre for Molecular Exercise Science, Hungarian University of Sport Science, Alkotas str. 44, Budapest, 1123, Hungary.
Dora AbrahamResearch Centre for Molecular Exercise Science, Hungarian University of Sport Science, Alkotas str. 44, Budapest, 1123, Hungary.
János FehérOphthalmology Unit, NESMOS Department, Faculty of Medicine and Psychology, Sant'Andrea Hospital, ''Sapienza'' University of Rome, Rome, Italy.
Zsolt RadakResearch Centre for Molecular Exercise Science, Hungarian University of Sport Science, Alkotas str. 44, Budapest, 1123, Hungary.
Azienda Ospedaliera Sant'Andrea · ITCentre for Social Sciences · HUUniversity of Tsukuba · JP

Funding

Hungarian Scientific Research Fund 112810National Excellence Program 126823TEKA, Hungarian University of Sports Science Grant 2022-Kolonics
6 · The paper itself

Abstract

backgroundIt has been suggested that exercise training and postbiotic supplement could decelerate the progress of functional and biochemical deterioration in double transgenic mice overexpresses mutated forms of the genes for human amyloid precursor protein (APP

methodsThirty-two adult APP/PS1

resultsWe found that exercise training decreased Alzheimer's Disease (AD)-related gene expression (NF-kB) that was not affected by postbiotic treatment. The preparation used for postbiotic treatment is composed of tyndallized Bifidobacterium longum and Lactobacillus acidophilus. Both of the postbiotics effectively disaggregated amyloid-β/Aβ-40 aggregates by chelating Zn

conclusionOur findings revealed distinct mechanisms behind improved memory performance in the whole brain: while exercise training modulates NF-kB signaling pathway regulating immune response until postbiotic diminishes APP gene expression, disaggregates pre-existing amyloid-β plaques and activates mitochondrial protein quality control in the region of brain out of hippocampus. Using the above treatments complements and efficiently slows down the development of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsATP-Dependent ProteasesBrainDisease Models, AnimalHippocampusHumansMaleMiceMice, TransgenicMitochondrial ProteinsNF-kappa BPlaque, AmyloidPresenilin-1Amyloid beta-PeptidesAmyloid beta-Protein PrecursorATP-Dependent ProteasesLONP1 protein, humanMitochondrial ProteinsNF-kappa BPresenilin-1Alzheimer’s diseaseBifidobacterium longumCognitive functionGut microbiotaLactobacillus acidophilusMetal ion chelationMitochondrial protein quality control

Identifiers

PMID38110905
PMCPMC10726509
OpenAlexW4389893165

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.