Evidence map›Paper›PMID 35953741›Full record

ArticleCellular and molecular neurobiology2023

Dietary Fiber Modulates the Release of Gut Bacterial Products Preventing Cognitive Decline in an Alzheimer's Mouse Model.

Daniel Cuervo-Zanatta, Tauqeerunnisa Syeda, Vicente Sánchez-Valle, Mariangel Irene-Fierro, Pablo Torres-Aguilar, Mónica Adriana Torres-Ramos, Mineko Shibayama-Salas, Angélica Silva-Olivares, Lilia G Noriega, Nimbe Torres and 5 more

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 66 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

15 authors at 5 institutions in 2 countries.

Daniel Cuervo-ZanattaLaboratorio de Neuroplasticidad y Neurodegeneración, Departamento de Farmacologia, Centro de Investigación y de Estudios Avanzados del I.P.N. (Cinvestav), Av. IPN 2508, Ciudad de Mexico, 07360, México.
Tauqeerunnisa SyedaLaboratorio de Neuroplasticidad y Neurodegeneración, Departamento de Farmacologia, Centro de Investigación y de Estudios Avanzados del I.P.N. (Cinvestav), Av. IPN 2508, Ciudad de Mexico, 07360, México.
Vicente Sánchez-ValleLaboratorio de Neuroplasticidad y Neurodegeneración, Departamento de Farmacologia, Centro de Investigación y de Estudios Avanzados del I.P.N. (Cinvestav), Av. IPN 2508, Ciudad de Mexico, 07360, México.
Mariangel Irene-FierroLaboratorio de Neuroplasticidad y Neurodegeneración, Departamento de Farmacologia, Centro de Investigación y de Estudios Avanzados del I.P.N. (Cinvestav), Av. IPN 2508, Ciudad de Mexico, 07360, México.
Pablo Torres-AguilarUnidad Periférica de Neurociencias, Instituto de Neurología y Neurocirugía Manuel Velasco Suárez (INNNMVS), Ciudad de Mexico, 14269, México.
Mónica Adriana Torres-RamosUnidad Periférica de Neurociencias, Instituto de Neurología y Neurocirugía Manuel Velasco Suárez (INNNMVS), Ciudad de Mexico, 14269, México.
Mineko Shibayama-SalasDepartmento de Infectómica y Patogénesis Molecular, Centro de Investigación y de Estudios Avanzados del I.P.N. (Cinvestav), Av. IPN 2508, 07360, Ciudad de Mexico, Mexico.
Angélica Silva-OlivaresDepartmento de Infectómica y Patogénesis Molecular, Centro de Investigación y de Estudios Avanzados del I.P.N. (Cinvestav), Av. IPN 2508, 07360, Ciudad de Mexico, Mexico.
Lilia G NoriegaDepartamento de Fisiología de la Nutrición, Instituto Nacional de Ciencias Médicas y de la Nutrición "Salvador Zubiran" (INCMNSZ), 14080, Ciudad de México, Mexico.
Nimbe TorresDepartamento de Fisiología de la Nutrición, Instituto Nacional de Ciencias Médicas y de la Nutrición "Salvador Zubiran" (INCMNSZ), 14080, Ciudad de México, Mexico.
Armando R TovarDepartamento de Fisiología de la Nutrición, Instituto Nacional de Ciencias Médicas y de la Nutrición "Salvador Zubiran" (INCMNSZ), 14080, Ciudad de México, Mexico.
Iván RuminotUniversidad San Sebastián, Facultad de Medicina y Ciencia, Centro de Estudios Científicos-CECs, Valdivia, Chile.
L Felipe BarrosUniversidad San Sebastián, Facultad de Medicina y Ciencia, Centro de Estudios Científicos-CECs, Valdivia, Chile.
Jaime García-MenaLaboratorio de Referencia y Soporte Para Genomas, Transcriptomas y Caracterización de Microbiomas, Departamento de Genética y Biología Molecular, Centro de Investigación y de Estudios Avanzados del I.P.N. (Cinvestav), Av. IPN 2508, Ciudad de Mexico, 07360, México. jgmena@cinvestav.mx.
Claudia Perez-CruzLaboratorio de Neuroplasticidad y Neurodegeneración, Departamento de Farmacologia, Centro de Investigación y de Estudios Avanzados del I.P.N. (Cinvestav), Av. IPN 2508, Ciudad de Mexico, 07360, México. cperezc@cinvestav.mx.
Center for Research and Advanced Studies of the National Polytechnic Institute · MXInstituto Politécnico Nacional · MXInstituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán · MXInstituto Nacional de Neurología y Neurocirugía · MXSan Sebastián University · CL

Funding

Centers of Excellence Basal Financing Program of ANID CECsConsejo Nacional de Ciencia y Tecnología 163235 INFR-2011-01Consejo Nacional de Ciencia y Tecnología A1S-42600SEP-Cinvestav Grant No.128
6 · The paper itself

Abstract

Fiber intake is associated with a lower risk for Alzheimer´s disease (AD) in older adults. Intake of plant-based diets rich in soluble fiber promotes the production of short-chain fatty acids (SCFAs: butyrate, acetate, propionate) by gut bacteria. Butyrate administration has antiinflammatory actions, but propionate promotes neuroinflammation. In AD patients, gut microbiota dysbiosis is a common feature even in the prodromal stages of the disease. It is unclear whether the neuroprotective effects of fiber intake rely on gut microbiota modifications and specific actions of SCFAs in brain cells. Here, we show that restoration of the gut microbiota dysbiosis through the intake of soluble fiber resulted in lower propionate and higher butyrate production, reduced astrocyte activation and improved cognitive function in 6-month-old male APP/PS1 mice. The neuroprotective effects were lost in antibiotic-treated mice. Moreover, propionate promoted higher glycolysis and mitochondrial respiration in astrocytes, while butyrate induced a more quiescent metabolism. Therefore, fiber intake neuroprotective action depends on the modulation of butyrate/propionate production by gut bacteria. Our data further support and provide a mechanism to explain the beneficial effects of dietary interventions rich in soluble fiber to prevent dementia and AD. Fiber intake restored the concentration of propionate and butyrate by modulating the composition of gut microbiota in male transgenic (Tg) mice with Alzheimer´s disease. Gut dysbiosis was associated with intestinal damage and high propionate levels in control diet fed-Tg mice. Fiber-rich diet restored intestinal integrity and promoted the abundance of butyrate-producing bacteria. Butyrate concentration was associated with better cognitive performance in fiber-fed Tg mice. A fiber-rich diet may prevent the development of a dysbiotic microbiome and the related cognitive dysfunction in people at risk of developing Alzheimer´s disease.

Indexed as

Alzheimer DiseaseCognitive DysfunctionGastrointestinal MicrobiomeNeuroprotective AgentsAnimalsButyratesDietary FiberDysbiosisMiceMice, TransgenicPropionatesButyratesDietary FiberNeuroprotective AgentsPropionates

Identifiers

PMID35953741
PMCPMC11412426
OpenAlexW4293288643

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.