Evidence map›Paper›PMID 36035436›Full record

ArticleBrain communications2022

Faecal microbiota transplant ameliorates gut dysbiosis and cognitive deficits in Huntington's disease mice.

Carolina Gubert, Jocelyn M Choo, Chloe J Love, Saritha Kodikara, Bethany A Masson, Jamie J M Liew, Yiwen Wang, Geraldine Kong, Vinod K Narayana, Thibault Renoir and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed.

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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

13 authors.

Carolina GubertFlorey Institute of Neuroscience and Mental Health, Melbourne Brain Centre, University of Melbourne, Parkville, VIC 3010, Australia.
Jocelyn M ChooMicrobiome and Host Health, South Australian Health and Medical Research Institute, Adelaide, SA 5001, Australia.
Chloe J LoveFlorey Institute of Neuroscience and Mental Health, Melbourne Brain Centre, University of Melbourne, Parkville, VIC 3010, Australia.
Saritha KodikaraMelbourne Integrative Genomics, School of Mathematics and Statistics, University of Melbourne, Parkville, VIC 3010, Australia.
Bethany A MassonFlorey Institute of Neuroscience and Mental Health, Melbourne Brain Centre, University of Melbourne, Parkville, VIC 3010, Australia.
Jamie J M LiewFlorey Institute of Neuroscience and Mental Health, Melbourne Brain Centre, University of Melbourne, Parkville, VIC 3010, Australia.
Yiwen WangMelbourne Integrative Genomics, School of Mathematics and Statistics, University of Melbourne, Parkville, VIC 3010, Australia.
Geraldine KongFlorey Institute of Neuroscience and Mental Health, Melbourne Brain Centre, University of Melbourne, Parkville, VIC 3010, Australia.
Vinod K NarayanaBio21 Institute and Department of Biochemistry and Molecular Biology, University of Melbourne, Parkville, VIC 3010, Australia.
Thibault RenoirFlorey Institute of Neuroscience and Mental Health, Melbourne Brain Centre, University of Melbourne, Parkville, VIC 3010, Australia.
Kim Anh Lê CaoMelbourne Integrative Genomics, School of Mathematics and Statistics, University of Melbourne, Parkville, VIC 3010, Australia.
Geraint B RogersMicrobiome and Host Health, South Australian Health and Medical Research Institute, Adelaide, SA 5001, Australia.
Anthony J HannanFlorey Institute of Neuroscience and Mental Health, Melbourne Brain Centre, University of Melbourne, Parkville, VIC 3010, Australia.ORCID https://orcid.org/0000-0001-7532-8922

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Huntington's disease is a neurodegenerative disorder involving psychiatric, cognitive and motor symptoms. Huntington's disease is caused by a tandem-repeat expansion in the huntingtin gene, which is widely expressed throughout the brain and body, including the gastrointestinal system. There are currently no effective disease-modifying treatments available for this fatal disorder. Despite recent evidence of gut microbiome disruption in preclinical and clinical Huntington's disease, its potential as a target for therapeutic interventions has not been explored. The microbiota-gut-brain axis provides a potential pathway through which changes in the gut could modulate brain function, including cognition. We now show that faecal microbiota transplant (FMT) from wild-type into Huntington's disease mice positively modulates cognitive outcomes, particularly in females. In Huntington's disease male mice, we revealed an inefficiency of FMT engraftment, which is potentially due to the more pronounced changes in the structure, composition and instability of the gut microbial community, and the imbalance in acetate and gut immune profiles found in these mice. This study demonstrates a role for gut microbiome modulation in ameliorating cognitive deficits modelling dementia in Huntington's disease. Our findings pave the way for the development of future therapeutic approaches, including FMT and other forms of gut microbiome modulation, as potential clinical interventions for Huntington's disease.

Indexed as

dementiagut microbiomeHuntington’s diseasemicrobiota–gut–brain axisneurodegenerative disorder

Identifiers

PMID36035436
PMCPMC9400176

What Socratic holds

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LicenceCC BY
Read underepoch 390

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.