# Amyotrophic Lateral Sclerosis: The State of the Art on Treatments and the Therapeutic Role of the Intestinal Microbiome in Human Studies

**Authors:** Ondřej Ptáček, Zdeněk Musil, Giulia Guarnieri, Alena Vrbacká, Pavla Moudrá, Aneta Zlámalová, Petra Röszlerová, Michal Tonhajzer, Vladimír Musil, Annamaria Morelli, Petr Zach

PMC · DOI: 10.3390/ijms27041655 · International Journal of Molecular Sciences · 2026-02-08

## TL;DR

This review examines the potential of fecal microbiota transplantation as a treatment for ALS, comparing results from three studies with mixed outcomes.

## Contribution

The paper provides a comparative analysis of existing human studies on FMT for ALS, highlighting methodological differences and their implications.

## Key findings

- Two studies observed halted ALS progression and improved health after FMT.
- One large study found no significant effect of FMT, possibly due to prior antibiotic use.
- Ongoing research is needed to clarify FMT's therapeutic effectiveness for ALS.

## Abstract

Amyotrophic lateral sclerosis (ALS) is a common neurodegenerative disorder; to date, there is no long-term effective treatment. Recently, a relationship has been discovered between the human intestinal microbiome and the pathogenesis of ALS, on which basis faecal microbiota transplantation (FMT) has been proposed as a potential treatment for ALS. In this review, we compare three existing case studies examining the effect of FMT on the course of ALS, highlighting differences in methodology and results. In two of the studies, a halt in the progression of ALS symptoms was observed following FMT, accompanied by improvement in patient health. However, in the third and largest study, no significant effect of FMT was observed. The possible explanation for this discrepancy may be the intentional depletion of intestinal microorganisms using antibiotics prior to FMT in the third study. Future studies and/or completion of the ongoing clinical studies will help clarify the therapeutic effectiveness of FMT in ALS patients.

## Linked entities

- **Diseases:** Amyotrophic lateral sclerosis (MONDO:0004976), ALS (MONDO:0004976)

## Full-text entities

- **Genes:** SOD1 (superoxide dismutase 1) [NCBI Gene 6647] {aka ALS, ALS1, HEL-S-44, IPOA, SOD, STAHP}, TARDBP (TAR DNA binding protein) [NCBI Gene 23435] {aka ALS10, TDP-43}, C9orf72 (C9orf72-SMCR8 complex subunit) [NCBI Gene 203228] {aka ALSFTD, DENND9, DENNL72, FTDALS, FTDALS1}, Sod1 (superoxide dismutase 1, soluble) [NCBI Gene 20655] {aka B430204E11Rik, Cu/Zn-SOD, CuZnSOD, Ipo-1, Ipo1, SODC}, FUS (FUS RNA binding protein) [NCBI Gene 2521] {aka ALS6, ETM4, FUS1, HNRNPP2, POMP75, TLS}
- **Diseases:** viral infection (MESH:D014777), arthritis (MESH:D001168), CDI (MESH:D003015), ALS (MESH:D000690), cough (MESH:D003371), dizziness (MESH:D004244), muscle tone (MESH:D009122), amyotrophy (MESH:D003929), infection (MESH:D007239), ischemic stroke (MESH:D002544), gastrointestinal and extraintestinal disorders (MESH:D005767), liver damage (MESH:D056486), constipation (MESH:D003248), dry mouth syndrome (MESH:D014987), bacterial infections (MESH:D001424), anxious and depressive symptoms (MESH:D003866), cognitive dysfunction (MESH:D003072), FTD (MESH:D057180), Multiple Sclerosis (MESH:D009103), sporadic ALS (MESH:C531617), pain (MESH:D010146), sleep disorders (MESH:D012893), head injury (MESH:D006259), Parkinson's disease (MESH:D010300), muscle stiffness (MESH:D019042), inflammation (MESH:D007249), atrophy of epiglottic muscles (MESH:D009133), neurodegenerative disease (MESH:D019636), injury to (MESH:D014947), autism (MESH:D001321), atrophied (MESH:D001284), neuroinflammation (MESH:D000090862), Alzheimer's disease (MESH:D000544), cancer (MESH:D009369), dysbiosis (MESH:D064806), Huntington's syndrome (MESH:D006816), weakness (MESH:D018908), fatigue (MESH:D005221), oesophageal paralysis (MESH:D010243), Sialorrhea (MESH:D012798), diarrhoea (MESH:D003967), Motor neuron disease (MESH:D016472), Chronic neuromuscular respiratory failure (MESH:D012131), skin cancer (MESH:D012878), nausea (MESH:D009325), loss of skeletal muscle strength (MESH:D005207), seizures (MESH:D012640)
- **Chemicals:** Na+ (MESH:D012964), PCO2 (-), baclofen (MESH:D001418), arginine (MESH:D001120), hyoscine hydrobromide (MESH:D012601), sodium butyrate (MESH:D020148), calcium (MESH:D002118), Riluzole (MESH:D019782), oxygen (MESH:D010100), Tofersen (MESH:C000709090), ciprofloxacin (MESH:D002939), coenzyme Q10 (MESH:C024989), metronidazole (MESH:D008795), vitamin E (MESH:D014810), nicotinamide (MESH:D009536), cholesterol (MESH:D002784), oligonucleotide (MESH:D009841), BCAA (MESH:D000597)
- **Species:** Turicibacter (genus) [taxon 191303], Clostridium (genus) [taxon 1485], Homo sapiens (human, species) [taxon 9606], Bacteria Latreille et al. 1825 (Bacteria stick insect, genus) [taxon 629395], Bacteroides (genus) [taxon 816], Bacillota (clostridial firmicutes, phylum) [taxon 1239], gut metagenome (species) [taxon 749906], Butyricimonas (genus) [taxon 574697], Dialister (genus) [taxon 39948], Lactobacillus (genus) [taxon 1578], Prevotella (genus) [taxon 838], Mus musculus (house mouse, species) [taxon 10090], Veillonella (genus) [taxon 29465], Enterobacter (genus) [taxon 547]
- **Mutations:** G93A

## Full text

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## References

61 references — full list in the complete paper: https://tomesphere.com/paper/PMC12941229/full.md

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Source: https://tomesphere.com/paper/PMC12941229