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Published on: June 2, 2022

Microplastics-Induced Gut Microbiota Dysbiosis Accelerates Alzheimer's-Like Pathology and Cognitive Decline via the

Zifeng Wu1, Jiarong Yang1, Miaoxuan Zhang1

  • 1Gansu Key Laboratory of Biomonitoring and Bioremediation for Environmental Pollution, and Ministry of Education Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|June 15, 2026
PubMed

Insights

Microplastics (MPs) accelerate Alzheimer's disease (AD) progression by disrupting gut bacteria and lowering taurine levels. Restoring taurine levels can reverse cognitive decline and neuroinflammation in AD mouse models.

Area of Science:

  • Neuroscience
  • Environmental Health
  • Microbiology

Background:

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder with no cure, increasingly linked to environmental factors.
  • Microplastics (MPs) are pervasive in the human diet, but their neurological effects remain largely uninvestigated.

Purpose of the Study:

  • To investigate the impact of chronic oral microplastic exposure on cognitive function and neurodegeneration in a mouse model of AD.
  • To elucidate the underlying mechanisms involving the gut-brain axis, microbiota, and metabolic changes.

Main Methods:

  • Chronic oral administration of amine-modified polystyrene microparticles to 5XFAD mice.
  • Assessment of cognitive decline, neuropathology (Aβ deposition, gliosis, synaptic loss), and autophagic flux.
  • Gut microbiota analysis, untargeted metabolomics, antibiotic treatment, and fecal microbiota transplantation (FMT).
  • Taurine level measurements in mouse plasma and human AD patient plasma (ADNI cohort).

Main Results:

  • Microplastic exposure accelerated cognitive decline, increased Aβ deposition, gliosis, synaptic loss, and impaired autophagic flux in 5XFAD mice.
  • MPs accumulated in the gut, altered microbiota composition (expanding Bilophila, suppressing commensals), leading to systemic taurine deficiency.
  • The neurotoxic effects were dependent on gut microbiota composition, as evidenced by antibiotic treatment and FMT studies.
  • Taurine restoration ameliorated neuropathology, restored autophagic flux, and rescued memory deficits.
  • Lower plasma taurine levels were observed in AD patients compared to controls and correlated inversely with cognitive decline.

Conclusions:

  • Microplastic-induced gut dysbiosis is a novel, modifiable environmental risk factor contributing to Alzheimer's disease pathogenesis.
  • Taurine deficiency resulting from gut dysbiosis exacerbates AD pathology via the gut-brain axis.
  • Taurine supplementation represents a promising, translatable therapeutic strategy to mitigate microplastic-induced neurodegeneration and AD progression.
Keywords:
Alzheimer's diseaseAβ pathologyTaurineautophagyfecal microbiota transplantationgut microbiotametabolomemicroplastics

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