Search Results (320)

The increased global prevalence of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), is a chronic relapsing inflammatory condition of the gastrointestinal tract that creates a substantial socioeconomic burden. Existing pharmacotherapeutic treatments primarily target inflammatory signaling cascades and have disadvantages because of the side effects of drugs, reduced long-term efficacy, and high cost, necessitating the development of safe and sustainable adjunctive therapies. This review synthesizes mechanistic advances regarding dietary polysaccharides as bioactive agents that may have the capacity to induce remodeling of inflamed gastrointestinal tract in colitis and could be an adjunctive strategy as functional food ingredients due to their various biological activities in the management of colitis. Polysaccharides alleviate colitis through several interconnected pathways. First, they correct the gut dysbiosis by enriching beneficial taxa such as Lactobacillus, Bifidobacterium, and Akkermansia muciniphila. Second, fermentation of polysaccharides produces short-chain fatty acids (SCFAs), particularly butyrate, which serve as the primary energy source for colonocytes. Third, they restore intestinal barrier integrity by upregulating tight junction proteins such as ZO-1, occludin, and claudin, also performing pro-inflammatory cascade inhibition and elimination of oxidative stress via Nrf2/HO-1 activation The relationship between structural properties of polysaccharides based on molecular weight, monosaccharide composition, and biological functions of chemically modified dietary polysaccharides in colitis is studied. Dietary polysaccharides are explored here not as replacements for pharmacotherapy but as potential adjunctive or functional food-based interventions that may complement existing treatments as safe, multitargeted, and cost-effective interventions in prevention or long-term management of colitis and IBD. This review presents dietary polysaccharides function not as passive dietary fibers but as bioactive, multi-targeted, structurally dependent agents capable of restoring intestinal homeostasis, suggesting them as potentially safe, adjunctive interventions. Full article

Background/Objectives: Acute lung injury (ALI) currently lacks safe and effective therapeutic strategies with low toxicity. Lonicerae japonicae flos, a traditional herb and functional food, contains polyphenols as its principal active components. This study investigated whether Lonicerae japonicae flos polyphenols (LJP) could exert protective effects against lipopolysaccharide (LPS)-induced ALI in mice. Methods: Eighty-four male C57BL/6J mice were randomly divided into seven groups and treated daily for 7 days with LJP (200, 100, or 50 mg/kg), liproxstatin-1 (10 mg/kg), dexamethasone (5 mg/kg), or saline (control and model groups). Subsequently, another thirty-six mice were used for the fecal microbiota transplantation (FMT) experiment. All groups except the control group received intratracheal instillation of LPS (5 mg/kg) to induce ALI. Results: LJP treatment significantly ameliorated lung histopathological damage and gut microbiota dysbiosis. Lung proteomics analysis revealed the enrichment of the NF-κB and ferroptosis pathways. Mechanistically, LJP downregulated pro-inflammatory factors (IL-6, TNF-α, and IL-1β) by suppressing activation of the TLR4/MyD88/NF-κB pathway. Meanwhile, LJP upregulated SOD and GSH levels, thereby suppressing the accumulation of ROS, GSSG, Fe²⁺, and MDA, which were closely related to the activation of the Nrf2/HO-1 and Sirt3/Nrf2/GPX4 pathways. Furthermore, LJP modulated the gut microbiota and promoted short-chain fatty acid (SCFA) production by elevating the relative abundance of Akkermansia muciniphila and Faecalibaculum. Intriguingly, FMT results confirmed that the LJP-derived gut microbiota markedly alleviated lung tissue injury and intestinal barrier damage in ALI mice. Conclusions: This study demonstrated that LJP could reshape the gut microbiota to enhance the production of SCFAs and inhibit inflammation-related ferroptosis in ALI mice. Full article

Background: Childhood obesity is increasingly associated with gut microbiome dysbiosis. This systematic review (PROSPERO CRD420251131354) evaluates evidence from studies published between 2020 and 2026 assessing how nutritional and lifestyle interventions influence gut microbiota in children with obesity. Methods: A systematic search of PubMed, EMBASE and EBSCO identified 21 interventional studies involving children aged 5–18 years with obesity, with the last search conducted in April 2026. Interventions comprised prebiotics, probiotics, synbiotics, postbiotics, high-fiber diets, calorie-restricted dietary approaches, and lifestyle modifications such as physical activity. Microbiome outcomes were analyzed using 16S rRNA sequencing, quantitative real-time polymerase chain reaction (qPCR), or metagenomics. Risk of bias was evaluated using the RoB 2 and ROBINS-I (version 2) tools. Due to substantial heterogeneity in study design, participant characteristics, intervention types, and analytical methods, a meta-analysis was not feasible. Results: Across 21 studies, nutritional interventions included measurable but heterogeneous alterations in gut microbiome composition. Inulin supplementation was associated with a significant increase in alpha diversity and with higher relative abundances of Bifidobacterium, Blautia, Megasphaera, Subdoligranulum, and Eubacterium coprostanoligenes. Synbiotic supplementation increased Prevotella and Dialister and reduced the Firmicutes/Bacteroidetes ratio. High-fiber dietary interventions increased Faecalibacterium, Bifidobacterium, and Clostridium, while reducing Bacteroides, and were associated with shifts in metabolic pathways related to carbohydrate, lipid, and nucleotide metabolism. Calorie-restricted diets and combined diet–exercise interventions increased beneficial taxa such as Akkermansia muciniphila, improved microbial diversity, and correlated with favorable metabolic and anthropometric outcomes. Overall, nutritional and lifestyle interventions in pediatric obesity were associated with taxon-specific and context-dependent microbiome changes, rather than uniform restructuring. Conclusions: Nutritional interventions can modulate gut microbiota diversity, composition, and predicted function in pediatric obesity; however, the observed effects vary substantially across studies. The limited number of trials, small sample sizes, and methodological heterogeneity underscore the need for larger, standardized studies to better define clinical and therapeutic implications. Full article

Cytolysin-positive Enterococcus faecalis is a key pathogen in severe alcoholic hepatitis, yet the mechanisms through which it worsens disease and possible therapeutic strategies remain poorly understood. This study aimed to clarify the pathogenic effects of E. faecalis in acute alcohol-associated liver disease (ALD) and to assess the protective potential of Akkermansia muciniphila (Akk11) against this pathogen. Using a mouse model of acute ethanol gavage, animals received E. faecalis and/or Akk11 under prophylactic or therapeutic regimens. Assessments included liver injury markers, histopathology, lipid profiles, inflammatory cytokines, gut barrier integrity, and gut microbiota composition. E. faecalis exacerbated ethanol-induced hepatic steatosis and injury, showing a paradoxical effect: it increased histological damage while lowering circulating LPS and transaminases. This was linked to upregulated hepatic autophagy (increased Atg7) and reduced cholesterol, yet it promoted neutral lipid accumulation. Importantly, E. faecalis aggravated gut dysbiosis by markedly enriching the pro-inflammatory pathobiont Helicobacter typhlonius and impairing colonic barrier function. Intervention with Akk11 alleviated liver injury, reduced lipid accumulation and oxidative stress, and restored cytokine balance. Akk11 also strengthened gut barrier integrity, lowered serum endotoxin, and beneficially reshaped the microbiota. Prophylactic administration was particularly effective, normalizing the Firmicutes/Bacteroidota ratio, suppressing H. typhlonius, and enriching beneficial Bacteroides sartorii. This study confirms the pathogenic role of E. faecalis in acute ALD and establishes A. muciniphila (Akk11) as a promising microbiota-targeted therapy, which protects against liver injury by reinforcing the gut barrier, selectively modulating microbiota, and reducing inflammation, with prophylactic administration showing superior efficacy. Full article

Background: The upper gastrointestinal (GI) tract is a complex environment characterized by sharp physicochemical gradients. While the oral microbiome is a major source of microbial seeding for downstream organs, it remains unclear how these communities correlate and diverge across different anatomical sites. This study provides a high-resolution re-analysis of a comprehensive multi-site dataset to delineate the microbial architecture and ecological signatures along the oral–upper GI axis. Method: Human oral, esophageal, gastric mucosal, and gastric juice microbiome sequencing data were retrieved from the publicly available National Center for Biotechnology Information (NCBI) BioProject PRJNA1049979 database. Using these publicly available 16S rRNA sequencing data, we performed an integrated ecological analysis. Microbial diversity, taxonomic composition, and niche-specific community structures were evaluated using Quantitative Insights Into Microbial Ecology 2 (QIIME2) and R-based tools, including linear discriminant analysis effect size (LEfSe) and phylogenetic mapping. Results: The esophageal microbiome showed significantly greater richness and evenness than the oral cavity and stomach. Beta diversity analysis demonstrated clear compositional separation between oral and downstream upper GI communities, whereas gastric samples, particularly gastric juice, showed greater heterogeneity. Although major phyla were shared across sites, their relative abundances differed markedly. Oral samples were enriched with periodontal-associated taxa, including Porphyromonas, Prevotella, Alloprevotella, and Fusobacterium. In contrast, gastric mucosal samples were enriched with Akkermansia muciniphila and Helicobacter pylori, whereas gastric juice was characterized by Sarcina ventriculi, Fusobacterium periodonticum, and Clostridium perfringens. These findings indicate both taxonomic continuity and pronounced site-specific ecological divergence along the oral–upper GI axis. Conclusion: The oral cavity, esophagus, stomach, and gastric juice share a common microbial framework but exhibit distinct community restructuring driven by local environmental selection. This study provides a detailed ecological view of the oral–upper GI microbiome and highlights the importance of site-specific microbial organization in upper GI health and disease. Full article

Lung cancer, particularly non-small cell lung cancer (NSCLC), remains the leading cause of cancer mortality worldwide. While immune checkpoint inhibitors (ICIs) have revolutionized treatment, primary and acquired resistance, and immune-related adverse events (irAEs) limit their therapeutic efficacy. Recent evidence highlights the gut and local microbial communities as a modifiable determinant of NSCLC outcomes, especially in the context of ICI use. Emerging data support the concept of a gut–lung-immune axis, a tridirectional communication pathway, in which gut and lung microbial communities influence local and systemic antitumor immunity through immune cell trafficking, cytokine signaling, and microbial-derived metabolites. In this review, we synthesize current clinical and mechanistic studies examining the role of gut, tumor-resident, and circulating microbiota in shaping ICI efficacy and toxicity in NSCLC. Distinct gut and tumor microbial signatures, such as the abundance of Akkermansia muciniphila and Bifidobacterium, correlate with improved ICI response, whereas dysbiosis promotes immune suppression, resistance, and irAEs. Additionally, we highlight emerging microbial-based biomarkers, including fecal microbial profiles, circulating microbial DNA, and composite tools such as TOPOSCORE, which show promise for predicting response, toxicity, and optimal treatment duration. Overall, these findings underscore the gut–lung-immune axis as a key regulator of immunotherapy outcomes in NSCLC and suggest that microbiome-informed strategies may enable more precise, effective, and safer personalization of ICI therapy. Full article

Background: Postbiotics, including cell-free supernatants and their fractions, have emerged as a safe and effective alternative to live probiotics for managing intestinal inflammation. This study investigated the protective effects of low-molecular-weight fractions (<3 kDa) of the probiotic Limosilactobacillus fermentum CECT5716 (LMW-LF) in a murine model of experimental colitis. Methods: Male C57BL/6J mice were orally administered LMW-LF for 10 days prior to colitis induction with 3% dextran sodium sulfate (DSS) for 5 days. Colonic damage was assessed via the Disease Activity Index (DAI), histology, and immunofluorescence (Ocln and Ki67). Immune cell populations were analyzed by flow cytometry, while mucosal gene expression and gut microbiota composition were evaluated using RT-qPCR and 16S rRNA sequencing, respectively. Results: LMW-LF administration significantly attenuated clinical symptoms and macroscopic colonic damage. Treatment restored epithelial barrier integrity by upregulating tight junction proteins (Tjp1) and mucin genes (Muc1-3) while normalizing DSS-induced epithelial hyperproliferation. Immunologically, LMW-LF reduced pro-inflammatory monocyte infiltration; downregulated Il6, Tnfa, and Ifng; and promoted an immunoregulatory phenotype by enhancing Ampk expression and partially restoring regulatory T cell (Treg) populations. Furthermore, LMW-LF reshaped the gut microbiota by increasing alpha diversity and promoting the enrichment of beneficial taxa, specifically Akkermansia muciniphila, which correlated with improved mucus layer preservation. Conclusions: LMW-LF is an active fraction acting across the host–microbiota axis. By integrating epithelial protection, immunomodulation, and microbial reshaping, it represents a promising dietary strategy for the management of Inflammatory Bowel Diseases. Full article

Obesity and type 2 diabetes mellitus (T2DM) represent intertwined global epidemics driven by gut dysbiosis, chronic inflammation, and impaired SCFA production, identifying the microbiome as a therapeutic target. This review synthesizes mechanistic insights and clinical evidence on the role of probiotics as microbiome modulators in the management of metabolic disease. A comprehensive literature search across PubMed, Scopus, Web of Science, and Google Scholar up to May 2026 identified ~230 records using keywords such as probiotics, SCFAs, obesity, and T2DM; a narrative synthesis integrated preclinical, RCT, and meta-analytic data without formal pooling due to heterogeneity. Probiotics restore eubiosis via strain-specific mechanisms, Lacticaseibacillus rhamnosus GG enhances tight junctions (ZO-1), Bifidobacterium breve BBr60 boosts butyrate cross-feeding, and pasteurized Akkermansia muciniphila remodels bile acids (FXR/FGF19), activating G-Protein Coupled Receptor 41 (GPR41)/43-GLP-1 signaling, Treg expansion, and NF-κB suppression. Beyond immunometabolic effects, probiotics mitigate obesity- and T2DM-related oxidative stress by upregulating endogenous antioxidant enzymes (e.g., SOD, catalase, GPx), modulating Nrf2/Keap1 signaling, and reducing lipid peroxidation and other oxidative stress markers in experimental and clinical settings. Meta-analyses of RCTs reveal modest benefits: BMI reductions (~0.3 kg m⁻²), waist circumference (WC) reductions (1–2 cm), HbA1c reductions (0.3–0.4%), and improvements in homeostatic model assessment of insulin resistance (HOMA-IR), especially with multi-strain (>10⁹ CFU day⁻¹, ≥12 weeks) synbiotics. Innovative strategies—synbiotics, postbiotics, AI-tailored consortia, and fermented dairy—address engraftment and response variability. Current guidelines recommend 10⁹–10¹¹ CFU day⁻¹ using multi-strain formulations for 12–24 weeks alongside lifestyle measures, with regimen selection tailored to the dysbiosis phenotype (e.g., NAFLD). Future longitudinal RCTs integrating multi-omics endpoints with AI-driven strain selection should refine—and ultimately individualize—precision probiotic strategies for metabolic therapy. Full article

Background: Polyphenols interact bidirectionally with the gut microbiota and may influence short-chain fatty acid (SCFA) production, yet evidence from human randomized controlled trials (RCTs) has not been comprehensively synthesized. Objectives: In this systematic review and meta-analysis, we evaluated the effects of polyphenol supplementation on gut microbiota composition, microbial diversity, and fecal SCFA concentrations in adults and examined moderators of these associations. Methods: Five databases were searched through October 2023 for RCTs assessing oral polyphenol supplementation in adults. Eligible studies reported outcomes related to gut microbiota composition or fecal SCFAs. Random-effects meta-analyses were conducted for SCFA outcomes, and subgroup analyses examined effects by polyphenol class, dose, duration, health status, and analytical methods. Risk of bias was assessed using the Cochrane RoB 2 tool, and certainty of evidence using GRADE. Results: Fifty RCTs (n = 2042 participants) were included. Polyphenol supplementation was associated with an increase in total SCFAs in 70.6% of studies and with significantly higher butyrate concentrations (pooled SMD = 0.48; 95% CI: 0.32–0.64; I² = 58%). Acetate and propionate increased in 75% and 71.4% of studies, respectively. A shift toward a more butyrogenic fermentation profile was observed. Polyphenol supplementation was associated with increases in the relative abundance of beneficial genera, including Bifidobacterium (81.8%), Akkermansia muciniphila (50%), and Faecalibacterium prausnitzii (45.5%), and with decreases in potentially pathogenic taxa such as Enterobacteriaceae and Clostridium spp. Increases in alpha diversity were reported in 66.7% of studies, and increases in beta diversity were reported in 87.5%. Associations tended to be stronger in individuals with metabolic disorders and in interventions lasting ≥12 weeks. Conclusions: Polyphenol supplementation is associated with favorable shifts in gut microbiota composition, higher fecal SCFA concentrations—particularly butyrate—and modest changes in microbial diversity. These findings should be interpreted as associations rather than evidence of mechanistic or prebiotic effects. Further mechanistic, dose-controlled, and long-term human studies are needed to determine whether these microbiota-related changes translate into clinically meaningful outcomes. Full article

The global burden of type 2 diabetes mellitus (T2DM) and metabolic dysfunction-associated steatotic liver disease (MASLD) continues to rise at an alarming pace, with substantial pathophysiological overlap driven by insulin resistance, visceral obesity, and chronic low-grade inflammation. MASLD may progress to metabolic dysfunction-associated steatohepatitis (MASH), with increased risk of cirrhosis and hepatocellular carcinoma. Glucagon-like peptide 1 (GLP-1)-based therapies have transformed the management of T2DM and obesity. They exert pleiotropic effects whose basis remains incompletely understood. Concurrently, Akkermansia muciniphila has emerged as a keystone gut microbiota species with demonstrated hepatoprotective potential in preclinical models of MASLD/MASH. This narrative review positions A. muciniphila simultaneously as a target of GLP-1-mediated microbiome remodeling and as an independent modulator of hepatoprotection in MASLD/MASH. A structured search of PubMed, Scopus, and Web of Science (last searched: 12 April 2026) was conducted using terms related to Akkermansia muciniphila, GLP-1 receptor agonists, MASLD/MASH and T2DM. A total of 174 records were identified. Of these, 148 were excluded due to duplication or non-relevant study design. 26 studies (23 preclinical, 3 clinical) were included in the synthesis, directly addressing A. muciniphila. Preclinical evidence demonstrates that liraglutide, semaglutide, exenatide, and tirzepatide increase A. muciniphila abundance, while A. muciniphila in turn enhances endogenous GLP-1 secretion via the P9/ICAM-2 axis, forming a hypothetical positive feedback loop. A working mechanistic model integrating these bidirectional interactions is proposed, alongside a discussion of current limitations and future research priorities, including microbiome-guided clinical trials in MASLD/MASH populations. Full article

Background: The gut microbiota constitutes a metabolically active “second genome” that profoundly modulates drug pharmacokinetics, pharmacodynamics, and adverse reaction profiles. Beyond antibiotics, widely prescribed non-antibiotic pharmacotherapies exert clinically relevant pharmacomicrobiomic effects with implications for therapeutic optimisation and pharmacovigilance. Methods: This narrative review, conducted following PRISMA 2020 reporting principles (without PROSPERO pre-registration), searched PubMed/MEDLINE, Scopus, Web of Science, and Cochrane Library (January 2015–December 2024) for evidence on proton pump inhibitors (PPIs), metformin, NSAIDs, statins, SGLT2 inhibitors, and oral iron. Evidence tables included clinical human studies with molecular microbiota characterisation (16S rRNA or shotgun metagenomics), ≥20 participants, and a control arm; preclinical data informed mechanistic synthesis. Results: Of 68 eligible studies, 20 met criteria for the evidence tables. PPIs significantly remodelled gut microbiota composition with enrichment of oral-origin taxa (“oralisation of the gut”), associating with Clostridioides difficile infection and SIBO. Metformin enriched Akkermansia muciniphila and butyrate producers, contributing causally to glycaemic efficacy. NSAIDs compromised barrier integrity, with synergistic dysbiosis under PPI co-prescription. Statins correlated with reduced prevalence of the dysbiotic Bact2 enterotype. SGLT2 inhibitor data remained discordant. Oral iron consistently enriched Enterobacteriaceae at the expense of beneficial commensals. Full article

Enteritis is a disease that affects Procambarus clarkii, significantly impacting aquaculture due to its high incidence and mortality rates, resulting in economic losses. Currently, the molecular mechanisms behind enteritis in Procambarus clarkii are not well understood. In this study, we established a model of intestinal inflammation induced by dextran sodium sulfate (DSS). Subsequently, histopathological changes, transcriptome analysis, intestinal microbiota analysis and immunofluorescence analysis were conducted. Histopathology showed that after treatment in the DSS + Narirutin (NR) group, there was an improvement in intestinal inflammation, and the structure of the intestinal tissue was partially restored. The intestinal transcriptome analysis revealed that in the DSS + NR group, 234 genes were upregulated and 188 genes were downregulated after treatment. This indicates a significant change in gene expression. KEGG enrichment analysis revealed that the DEGs were significantly enriched in TGF-β signaling pathway and PI3K-Akt signaling pathway. The results from 16S rRNA sequencing showed that in the DSS + NR group, the relative abundance of Akkermansia muciniphila significantly increased. Immunofluorescence results showed that, compared to the control group, the expressions of Occludin, nuclear factor-kB-p65 (NfkB-p65), Zonula occludens-1 (ZO-1), and Claudin-1 decreased following DSS treatment. However, treatment with NR was able to inhibit these changes. This further validated that NR can alleviate enteritis in Procambarus clarkii. Full article

With colorectal cancer (CRC) accounting for over 1.9 million new cases and 930,000 deaths globally in 2020, there is a critical need for innovative indicators to forecast disease advancement and therapeutic outcomes. The gut microbiome has emerged as a fertile area for discovering such diagnostic and prognostic signals. This narrative review collected current evidence on intestinal microorganisms and their metabolic products as candidate markers for CRC control. Intestinal communities influence malignancy through diverse mechanisms, including metabolic shifts, immune modulation, inflammation, proliferation/apoptosis regulation, genotoxicity, and mucosal barrier disruption. Pathogenic species, such as Fusobacterium nucleatum and enterotoxigenic Bacteroides fragilis, facilitate tumorigenesis via FadA-mediated signaling and Th17/IL-17 responses. In contrast, beneficial taxa like Faecalibacterium prausnitzii and Akkermansia muciniphila provide protective effects through short chain fatty acid production. Macrophage phenotype physiological equilibrium is altered and inflammatory status fluctuates under the former. Metabolically, hydrogen sulfide damages mitochondrial DNA and secondary bile acids stimulate cellular proliferation. While 16S rRNA sequencing and shotgun metagenomics are established detection strategies, innovative platforms like organoids and gene arrays remain in the exploratory stage. Clinical data indicates that F. nucleatum aligns with advanced tumor stage, and its combined detection with colibactin-producing E. coli achieves high sensitivity for early-stage screening. Additionally, A. muciniphila levels can anticipate the efficacy of PD-1 blockade immunotherapy. Microbiota-derived tools represent a transformative direction in oncology. Future research must focus on standardizing protocols and validating multi-marker panels to enhance clinical translation. Full article

The skin is a complex immunological organ in which reactive oxygen species (ROS)-related pathways and host–microbe interactions synergically maintain immune homeostasis. Dysregulation of several oxidative mechanisms, including lipid peroxidation, mitochondrial dysfunction, ferroptosis, and impaired antioxidant defenses, alongside gut microbiome imbalance, is increasingly recognized as a key modulator of the immune response involved in disease onset and progression. However, their role in immune-mediated dermatoses remains incompletely defined. This narrative review aims to provide a comprehensive overview of the contribution of these altered pathways to the pathogenesis and prognosis of the major immune-mediated skin diseases. Across all conditions examined, elevated oxidative biomarkers, such as malondialdehyde (MDA), advanced glycation end-products (AGEs), advanced oxidation protein products (AOPPs), 8-hydroxydeoxyguanosine (8-OHdG), and reduced antioxidant capacity are consistently reported. Ferroptosis, driven by iron-dependent lipid peroxidation and dysfunction of Glutathione peroxidase 4 (GPX4), emerges as a relevant cell death pathway, particularly in psoriasis and atopic dermatitis (AD). In parallel, dysbiosis of the gut and skin microbiomes, characterized by depletion of short-chain fatty acid (SCFA)-producing taxa such as Faecalibacterium prausnitzii, Bifidobacterium, and Akkermansia muciniphila, has been reported across multiple diseases. Particular attention is given to shared molecular axes, such as the disruption of epithelial barrier integrity, activation of innate and adaptive immune responses, and the role of microbial-derived metabolites in modulating redox signaling, unraveling a bidirectional crosstalk. Emerging therapeutic strategies targeting these bidirectional crosstalks show biological plausibility and promising preliminary results. Integrating redox and microbial profiling into clinical practice may improve patient stratification and foster the development of more personalized therapeutic approaches beyond conventional immunological treatments. Full article

Akkermansia muciniphila (A. muciniphila) is a bacterium that breaks down mucus and is studied for its effects on metabolism and the immune system. Studies show that it affects Alzheimer’s disease (AD) by protecting the gut barrier, reducing inflammation, and influencing communication between the immune system, the brain, and mitochondria. This review summarizes mechanistic, preclinical, and translational evidence connecting A. muciniphila to AD, including products such as short-chain fatty acids (SCFAs), and structural or secreted proteins including Amuc_1100 and extracellular vesicles (AmEVs). We also discuss differences between bacterial strains, differences in research methods, and findings that change under different conditions, which make the results harder to interpret. Animal studies suggest neuroprotective effects, but clinical evidence is still limited. Clinical use will need human studies at the strain level, confirmation in humanized models, and early trials using biomarkers to test safety and causal effects. Full article