Evidence map›Paper›PMID 39461991›Full record

ArticleScientific reports2024

Brazilian kefir fraction mitigates the Alzheimer-like phenotype in Drosophila melanogaster with β-amyloid overexpression model.

Serena Mares Malta, Tamiris Sabrina Rodrigues, Matheus Henrique Silva, Alexandre Souza Marquez, Rafael Bernardes Ferreira, Fernanda Naves Araújo do Prado Mascarenhas, Renata Graciele Zanon, Lucas Matos Martins Bernardes, Letícia Leandro Batista, Murillo Néia Thomaz da Silva and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

15 authors.

Serena Mares MaltaLaboratory of Genetics, Institute of Biotechnology, Federal University of Uberlândia, Acre Street, 2E building, room 230, Uberlândia, MG, 38405-319, Brazil. serena@ufu.br.
Tamiris Sabrina RodriguesLaboratory of Genetics, Institute of Biotechnology, Federal University of Uberlândia, Acre Street, 2E building, room 230, Uberlândia, MG, 38405-319, Brazil.
Matheus Henrique SilvaLaboratory of Genetics, Institute of Biotechnology, Federal University of Uberlândia, Acre Street, 2E building, room 230, Uberlândia, MG, 38405-319, Brazil.
Alexandre Souza MarquezLaboratory of Genetics, Institute of Biotechnology, Federal University of Uberlândia, Acre Street, 2E building, room 230, Uberlândia, MG, 38405-319, Brazil.
Rafael Bernardes FerreiraLaboratory of Genetics, Institute of Biotechnology, Federal University of Uberlândia, Acre Street, 2E building, room 230, Uberlândia, MG, 38405-319, Brazil.
Fernanda Naves Araújo do Prado MascarenhasInstitute of Biomedical Sciences, Federal University of Uberlândia, Uberlândia, MG, Brazil.
Renata Graciele ZanonInstitute of Biomedical Sciences, Federal University of Uberlândia, Uberlândia, MG, Brazil.
Lucas Matos Martins BernardesLaboratory of Genetics, Institute of Biotechnology, Federal University of Uberlândia, Acre Street, 2E building, room 230, Uberlândia, MG, 38405-319, Brazil.
Letícia Leandro BatistaInstitute of Developmental Biology and Neurobiology, Johannes Gutenberg University Mainz, Mainz, Germany.
Murillo Néia Thomaz da SilvaInstitute of Chemistry, Federal University of Uberlândia, Uberlândia, MG, Brazil.
Débora de Oliveira SantosFaculty of Odontology, Federal University of Uberlândia, Uberlândia, MG, Brazil.
Ana Carolina Costa SantosLaboratory of Genetics, Institute of Biotechnology, Federal University of Uberlândia, Acre Street, 2E building, room 230, Uberlândia, MG, 38405-319, Brazil.
Ana Paula Mendes-SilvaDepartment of Psychiatry, University of Saskatchewan, Saskatoon, SK, Canada.
Foued Salmen SpindolaLaboratory of Genetics, Institute of Biotechnology, Federal University of Uberlândia, Acre Street, 2E building, room 230, Uberlândia, MG, 38405-319, Brazil.
Carlos Ueira-VieiraLaboratory of Genetics, Institute of Biotechnology, Federal University of Uberlândia, Acre Street, 2E building, room 230, Uberlândia, MG, 38405-319, Brazil. ueira@ufu.br.

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
Conselho Nacional de Desenvolvimento Científico e Tecnológico 312812/2021-3Conselho Nacional de Desenvolvimento Científico e Tecnológico 403193/2022-2Fundação de Amparo à Pesquisa do Estado de Minas Gerais APQ-00269-22Fundação de Amparo à Pesquisa do Estado de Minas Gerais APQ-02766-17NIH HHS P40 OD018537
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative condition and the primary form of dementia among elderly people. The amyloidogenic hypothesis is the main theory that explains this phenomenon and describes the extracellular accumulation of amyloid beta (Aβ) peptides. Model organisms such as Drosophila melanogaster have been utilized to improve the understanding of this disease and its treatment. This study evaluated the effects of peptide and metabolic fractions of Brazilian kefir on a strain of D. melanogaster that expresses human Aβ peptide 1-42 in the eye. The parameters assessed included ommatidial organization, vacuole area, retinal thickness, and Aβ peptide quantification. The present study revealed that the fractions, particularly the peptidic fraction, significantly reduced the vacuole area and increased the retina thickness in treated flies, indicating an improvement in neurodegeneration phenotype. The peptidic fraction was also found to alter Aβ aggregation dynamics, inhibiting Aβ fibril formation, as revealed by dynamic light scattering. This study demonstrated that kefir fractions, particularly the peptidic fraction < 10 kDa, have the potential to regulate Aβ aggregation and alleviate neurodegeneration in a Drosophila melanogaster AD-like model. These findings suggest that kefir fractions could be viable for the bioprospection of novel drug prototypes for AD treatment, providing valuable insights into strategies targeting Aβ aggregation and neurodegeneration in AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesDisease Models, AnimalDrosophila melanogasterKefirAnimalsBrazilHumansPeptide FragmentsPhenotypeAmyloid beta-Peptidesamyloid beta-protein (1-42)Peptide FragmentsAlzheimer’s diseaseDrosophila melanogasterKefir fractions

Identifiers

PMID39461991
PMCPMC11513133

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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.