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Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Environmental Sources Food & Water Gut & Microbiome Human Health Effects Nanoplastics Sign in to save

Cerebral to SystemicRepresentations of Alzheimer’sPathogenesis Stimulated by Polystyrene Nanoplastics

Figshare 2025
Yue Wang (65477), Xiufang Liang (16838776), Nicholas Andrikopoulos (10994835), Shufang Zheng (1755142), Yuhuan Li (337260), Pu Chun Ke (456097)

Summary

Researchers exposed both wild-type and APP/PS1 Alzheimer's model mice to environmental levels of polystyrene nanoplastics and measured Alzheimer's-like pathology progression. Nanoplastics exacerbated cognitive decline, microglial activation, and hippocampal neuronal death, particularly in the Alzheimer's model, with systemic inflammatory effects suggesting plastic particles may accelerate neurodegeneration.

Polymers
Models

Plastics discharged into the ecosphere can transform into micro- and nanoparticles to instigate interactions with biosystems, posing a threat to environmental sustainability and human health. While nanoplastics have recently been identified in abundance in the human brain, especially in the decedent brain tissues of dementia subjects, how these exogenous miniatures mediate neurological as well as systemic pathologies remains unclear. Here, we first investigated how environmental-level nanoplastic exposure influences the progression of Alzheimer’s disease, from cerebral to systemic representations. Specifically, polystyrene nanoplastics aggravated Alzheimer’s-like symptoms in both wild-type and APP/PS1 mice and stimulated microglial activation and hippocampal neuronal death, accentuated by peripheral abnormalities of lipid accumulation, hepatic steatosis, inflammation, adipocyte enlargement, and gut microbiota imbalance. These findings implicate that nanoplastic-induced neurological damage is not confined within the brain but expands systemically through the gut–liver–brain axis, thereby contributing to the multiscale and multidirectional progression of Alzheimer’s pathophysiology.

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