Evidence map›Paper›PMID 28129947›Full record

ArticleClinical therapeutics2017

Target Intestinal Microbiota to Alleviate Disease Progression in Amyotrophic Lateral Sclerosis.

Yong-Guo Zhang, Shaoping Wu, Jianxun Yi, Yinglin Xia, Dapeng Jin, Jingsong Zhou, Jun Sun

Abstract read
In one paragraph

Article in Clinical therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed, 6 pooled it
–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

140 citing papers in PubMed, 6 syntheses or guidelines pooled it.

  1. Pooled it
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  6. Pooled it
  7. Trial
  8. Review
  9. The microbiota-proteostasis axis: implications in neurodegenerative diseases.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Review
  10. Article
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  12. Article
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  15. Systemic brain-body metabolic coupling patterns in amyotrophic lateral sclerosis: a whole-body [European journal of nuclear medicine and molecular imaging · 2026
    Article
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80 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Yong-Guo ZhangDivision of Gastroenterology and Hepatology, Department of Medicine, University of Illinois, Chicago, Illinois.
Shaoping WuDepartment of Biochemistry, Rush University Medical Center, Chicago, Illinois.
Jianxun YiDepartment of Physiology, Kansas City University of Medicine and Bioscience, Kansas City, Missouri.
Yinglin XiaDivision of Gastroenterology and Hepatology, Department of Medicine, University of Illinois, Chicago, Illinois.
Dapeng JinDivision of Gastroenterology and Hepatology, Department of Medicine, University of Illinois, Chicago, Illinois.
Jingsong ZhouDepartment of Physiology, Kansas City University of Medicine and Bioscience, Kansas City, Missouri.
Jun SunDivision of Gastroenterology and Hepatology, Department of Medicine, University of Illinois, Chicago, Illinois. Electronic address: junsun7@uic.edu.

Funding

Vitamin D Receptor Regulation of Microbiota in Intestinal EpitheliaR01DK105118 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SUN, JUN · 2016 to 2020
$1.8M
Ca Signaling in Progression of Amyotrophic Lateral Sclerosis in Skeletal MuscleR01AR057404 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI ZHOU, JINGSONG · 2010 to 2014
$1.6M
NIAMS NIH HHS R01 AR057404NIDDK NIH HHS R01 DK105118
6 · The paper itself

Abstract

purposeEmerging evidence has demonstrated that gut microbiome plays essential roles in the pathogenesis of human diseases in distal organs. Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the progressive loss of motor neurons. Treatment with the only drug approved by the US Food and Drug Administration for use in ALS, riluzole, extends a patient׳s life span by only a few months. Thus, there is an urgent need to develop novel interventions that for alleviate disease progression and improve quality of life in patients with ALS. Here we present evidence that intestinal dysfunction and dysbiosis may actively contribute to ALS pathophysiology.

methodsWe used G93A transgenic mice as a model of human ALS. The G93A mice show abnormal intestinal microbiome and damaged tight junctions before ALS disease onset. The mice were given 2% butyrate, a natural bacterial product, in the drinking water.

resultsIn mice fed with butyrate, intestinal microbial homeostasis was restored, gut integrity was improved, and life span was prolonged compared with those in control mice. At the cellular level, abnormal Paneth cells-specialized intestinal epithelial cells that regulate the host-bacterial interactions-were significantly decreased in the ALS mice treated with butyrate. In both ALS mice and intestinal epithelial cells cultured from humans, butyrate treatment was associated with decreased aggregation of the G93A superoxide dismutase 1 mutated protein. IMPLICATIONS: The findings from this study highlight the complex role of the gut microbiome and intestinal epithelium in the progression of ALS and present butyrate as a potential therapeutic reagent for restoring ALS-related dysbiosis.

Indexed as

Gastrointestinal MicrobiomeAmyotrophic Lateral SclerosisAnimalsDisease Models, AnimalDisease ProgressionHumansMiceMice, TransgenicMotor NeuronsQuality of LifeSuperoxide DismutaseSOD1 G93A proteinSuperoxide DismutaseALSbutyratedysbiosisintestinal permeabilitymicrobiometight junctions

Identifiers

PMID28129947
PMCPMC5344195

What OpenQuestion holds

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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 OpenQuestion graph.