Summary of gut microbiota variations in ASD, epilepsy/DRE, and SCZ.
| Condition | Increased abundance | Reduced abundance | Related findings | References |
|---|---|---|---|---|
| ASD | -Firmicutes-Bacteroides-Pseudomonadota-Clostridium spp.-Desulfovibrio-Sutterella | -Bacteroidetes-Bifidobacterium-Prevotella | -Dysbiosis with low-grade inflammation.-Increased propionic acid and altered SCFAs profiles.-SCFAs modulation of DA and 5-HT in neuronal gene expression and monoaminergic pathways.-Changes in tryptophan metabolites.-Metabolite alterations correlate with GI symptoms and behavioral scores. | [135, 136, 141–144]. |
| Epilepsy and DRE | -Firmicutes (↑ in DRE)-Actinobacteria-Blautia -Subdoligranulum-Bifidobacterium (↑ in DRE and after KD)-Clostridiales-Bacteroides (↑ after KD)-Prevotella (↑ after KD) | -Bacteroidetes-Proteobacteria (variable)-Lactobacillales-Bifidobacterium (variable) | -Overall reduced alpha diversity.-Dysbiosis with altered B:F ratio.-Altered GABA, 5-HT, NE, and DA-producing bacteria.-Pro-inflammatory gut environment.-Stress-induced “leaky gut”.-DRE-associated dysbiosis linked to pharmacoresistance and seizure frequency.-KD remodels the microbiota (↑ Bacteroides, Prevotella, Bifidobacterium; ↓ Firmicutes; partial normalization of F:B ratio).-KD-associated ≥ 50% seizure reduction. | [21, 22, 49–51, 102, 119, 145–153]. |
| SCZ | -Lactobacillus-Prevotella-Akkermansia-Clostridium-Bacteroides-Escherichia/Shigella-Ruminococcus gnavus-Alistipes (propionate-producing) | -Faecalibacterium-Roseburia-Coprococcus-Ruminococcus bromii(All associated with reduced butyrate production, higher IL-6 and greater clinical severity) | -Altered B:F ratio.-Higher abundance of taxa linked to immune activation.-Reduced microbial pathways for butyrate synthesis.-Increased microbial pathways for propionate and succinate production.-Reduced alpha diversity.-Increased mucin degradation leading to “leaky gut”.-Greater translocation of LPS.-Prevotella-derived succinate and TCA-cycle intermediates.-Elevated pro-inflammatory cytokines (IL-6, IL-1β).-Decreased SCFAs. | [23, 24, 154–157]. |
The table outlines bacterial taxa with increased or reduced abundance in each condition, the associated metabolic or immunological findings, and key references supporting these observations. Notable patterns include shifts in the F:B ratio, alterations in SCFA-producing species, increased pro-inflammatory taxa, and changes linked to gut permeability, neurotransmitter pathways, and systemic neuroinflammation. ASD: autism spectrum disorder; DRE: drug-resistant epilepsy; SCZ: schizophrenia; KD: ketogenic diet; SCFAs: short-chain fatty acids; DA: dopamine; 5-HT: serotonin; GABA: γ-aminobutyric acid; NE: norepinephrine; LPS: lipopolysaccharide; TCA: tricarboxylic acid cycle; B:F ratio: Bacteroidetes:Firmicutes ratio.
ECLL: Investigation, Writing—original draft, Writing—review & editing, Validation, Supervision. RMP: Investigation, Writing—original draft, Writing—review & editing. GCH: Conceptualization, Investigation, Writing—original draft, Writing—review & editing, Visualization. MFBG: Conceptualization, Investigation, Writing—original draft. AMV: Conceptualization, Investigation, Writing—original draft. XAVT: Conceptualization, Investigation, Writing—original draft. ESA: Conceptualization, Investigation, Writing—original draft, Writing—review & editing. EJGA: Conceptualization, Investigation, Writing—original draft, Writing—review & editing. PCMP: Conceptualization, Writing—original draft, Writing—review & editing. DDLV: Investigation, Writing—original draft. LMG: Investigation, Writing—original draft. IVAA: Writing—review & editing, Validation. FES: Conceptualization, Investigation, Writing—original draft, Writing—review & editing. All authors read and approved the submitted version.
The authors declare that they have no conflicts of interest.
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This paper represents independent research supported by Universidad Anáhuac México. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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