Advanced science (Weinheim, Baden-Wurttemberg, Germany)Jun 15, 2026

Microplastics disrupt gut bacteria and may speed up Alzheimer's-like brain changes and memory loss through gut-brain communication

Gut-Brain Axis Weekly Brief ↗PubMed ↗DOI ↗OA ↗

Updated Jun 16, 2026

Abstract

Chronic oral exposure to 2-µm amine-modified polystyrene microparticles accelerates cognitive decline in 5XFAD mice.

Ingested microplastics accumulate in the gut and disrupt the gut barrier.
Exposure to microplastics leads to an increase in amyloid-beta deposition, gliosis, and synaptic loss.
A systemic taurine deficit is observed that correlates with increased neurodegenerative markers in the mice.
Microbiota disturbances caused by microplastics contribute to the neurotoxic effects, as shown by microbiota ablation and fecal microbiota transplantation.
Restoring taurine levels can improve microglial function and memory deficits associated with microplastic exposure.
Taurine levels are significantly lower in Alzheimer's disease patients compared to cognitively normal individuals.

Simplified

Alzheimer's disease (AD) is incurable and increasingly attributed to gene-environment interactions. Microplastics (MPs) are omnipresent in the human food chain, yet their impact on neurodegeneration is largely unknown. Here we show that chronic oral exposure to 2-µm amine-modified polystyrene microparticles accelerates cognitive decline, amplifies Aβ deposition, gliosis, and synaptic loss, and cripples autophagic flux in 5XFAD mice through the gut-brain axis. MPs accumulate in the gut, breach the epithelial barrier, and selectively expand the taurine-depleting pathobiont Bilophila, while suppressing taurine-synthesizing commensals. Untargeted metabolomics reveal a systemic taurine deficit that precedes and predicts exacerbated Aβ deposition, gliosis, synaptic loss, and autophagic blockade in 5XFAD mice. Antibiotic-mediated microbiota ablation and fecal microbiota transplantation (FMT) demonstrate that the neurotoxic phenotype is fully microbiota-dependent. Restoring taurine level rebalances microglial homeostasis, reinstates autophagic flux, and rescues memory deficits in MPs-treated 5XFAD mice. Translational validation using Alzheimer's Disease Neuroimaging Initiative (ADNI) plasma shows taurine is significantly lower in AD patients versus cognitively normal controls and inversely correlates with cognitive decline. Our findings identify MPs-induced gut-microbiota dysbiosis as a modifiable environmental driver of AD pathogenesis and establish taurine supplementation as a readily translatable intervention that simultaneously fortifies the intestinal barrier and neutralizes microbiota-mediated neurodegeneration.