# Effects and Mechanisms of Probiotics, Prebiotics, Synbiotics, and Postbiotics for the Prevention and Management of Alzheimer’s Disease: A Narrative Review

**Authors:** Ting Chen, Haoqi Chen, Yingzhen Qiu, Yixiao Liu, Mengxing Xie, Siyu Huang, Kaiying Feng, Jie Zhuang, Lu Chen, Yanming Chen, Huabin Li, Mengtao Yang, Zhijun Yang, Huilian Zhu

PMC · DOI: 10.3390/antiox15030347 · Antioxidants · 2026-03-10

## TL;DR

This review explores how probiotics, prebiotics, synbiotics, and postbiotics may help prevent or manage Alzheimer’s disease by influencing the gut-brain axis.

## Contribution

The paper provides a comprehensive synthesis of recent evidence on the mechanisms and effects of microbiota-targeted interventions for Alzheimer’s disease.

## Key findings

- PPSPs improve cognitive performance and reduce AD pathology via gut microbiota modulation and neuroinflammation reduction.
- PPSPs decrease amyloid-beta deposition and tau hyperphosphorylation while promoting synaptic plasticity.
- Variability in outcomes is linked to factors like strain specificity, dosage, and patient heterogeneity.

## Abstract

Alzheimer’s disease (AD) is a rapidly escalating global health crisis with limited effective treatments. Emerging research underscores the pivotal role of the microbiota–gut–brain axis in AD pathogenesis, prompting the exploration into gut microbiota-targeted interventions. This narrative review aimed to comprehensively synthesize the latest epidemiological, experimental, and clinical evidence regarding the effects and mechanisms of probiotics, prebiotics, synbiotics, and postbiotics (PPSPs) in AD prevention and management. We conducted a narrative review of relevant literature from the Web of Science and PubMed databases. The search focused on articles published within the last 5 years using keywords such as “Alzheimer’s disease”, “AD”, “gut-brain axis”, “gut microbiota”, “probiotics”, “prebiotics”, “synbiotics”, and “postbiotics”. The findings suggest that PPSPs mitigate AD pathology and improve cognitive performance by modulating gut microbiota, strengthening intestinal barrier integrity, decreasing amyloid-beta (Aβ) deposition and tau hyperphosphorylation, reducing neuroinflammation and oxidative stress, regulating neurotransmitter metabolism, and promoting synaptic plasticity. Some studies also report varied outcomes, attributable to factors like strain specificity, dosage, intervention duration, patient heterogeneity, and methodological differences. In conclusion, targeting the microbiota–gut–brain axis with PPSPs offers a promising, mechanism-based strategy for AD, though further research is essential to optimize specific interventions for clinical application.

## Linked entities

- **Diseases:** Alzheimer’s disease (MONDO:0004975)

## Full-text entities

- **Genes:** APP (amyloid beta precursor protein) [NCBI Gene 351] {aka AAA, ABETA, ABPP, AD1, APPI, CTFgamma}, MAPT (microtubule associated protein tau) [NCBI Gene 4137] {aka DDPAC, FTD1, FTDP-17, MAPTL, MSTD, MTBT1}
- **Diseases:** neuroinflammation (MESH:D000090862), AD (MESH:D000544)
- **Chemicals:** Prebiotics (MESH:D056692), Postbiotics (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC13024051/full.md

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13024051/full.md

## References

103 references — full list in the complete paper: https://tomesphere.com/paper/PMC13024051/full.md

---
Source: https://tomesphere.com/paper/PMC13024051