Fecal Microbiota Transplantation in Alzheimer’s Disease: Mechanistic Insights Through the Microbiota–Gut–Brain Axis and Therapeutic Prospects

Aug 28, 2025Microorganisms

Fecal Microbiota Transplantation and Its Possible Role in Alzheimer's Disease Through Gut-Brain Connections and Treatment Potential

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Abstract

Fecal microbiota transplantation (FMT) has shown potential to reduce amyloid-β plaques and normalize tau phosphorylation in Alzheimer's disease animal models.

Dysregulation of gut microbiota composition is associated with increased neuroinflammation and progression of Alzheimer's disease.
Restoring microbial balance may provide a therapeutic strategy for mitigating Alzheimer's disease symptoms.
Preclinical studies suggest that FMT can ameliorate cognitive deficits and neuropathology linked to Alzheimer's disease.
FMT has been shown to suppress inflammasome activation and restore microglial function through changes in microbial metabolites.
Current clinical evidence for FMT's effects in Alzheimer's disease is limited to case reports and small-scale trials.

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Alzheimer's disease (AD), a prevalent neurodegenerative disorder in the aging population, remains without definitive therapeutic solutions. Emerging insights into the gut microbiota (GM) and its bidirectional communication with the central nervous system(CNS) through the microbiota-gut-brain axis (MGBA) have unveiled potential correlative mechanisms that may contribute to AD pathogenesis, though causal evidence remains limited. Dysregulation of GM composition (dysbiosis) exacerbates AD progression via neuroinflammation, amyloid-β (Aβ) deposition, and tau hyperphosphorylation (p-tau), while restoring microbial homeostasis presents a promising therapeutic strategy. Fecal microbiota transplantation (FMT), a technique to reconstitute gut ecology by transferring processed fecal matter from healthy donors, has demonstrated efficacy in ameliorating cognitive deficits and neuropathology in AD animal models. Preclinical studies reveal that FMT reduces Aβ plaques, normalizes tau phosphorylation, suppresses inflammasome activation, and restores microglial homeostasis through modulation of microbial metabolites and immune pathways. Although clinical evidence remains limited to case reports and small-scale trials showing potential therapeutic effect, safety concerns regarding long-term effects and protocol standardization necessitate further investigation. This review synthesizes current knowledge on GM-AD interactions, evaluates FMT's mechanistic potential, and discusses challenges in translating this ancient practice into a cutting-edge AD therapy. Rigorous randomized controlled trials and personalized microbiota-based interventions are imperative to advance FMT from bench to bedside.

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Fecal Microbiota Transplantation in Alzheimer’s Disease: Mechanistic Insights Through the Microbiota–Gut–Brain Axis and Therapeutic Prospects

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