PD-like pathogenesis induced by intestinal exposure to microplastics: An in vivo study of animal models to a public health survey

With the increasing incidence of non-hereditary Parkinson's disease (PD), research into the involvement of specific environmental factors, in addition to aging, has become more prominent. The effects of microplastic exposure on public health have gained increased attention as it is known to cause a range of neurotoxic changes, some of which are similar to the pathological features of PD. We carried out low-dose microplastic exposure experiments on mice and Caenorhabditis elegans models and implemented a survey regarding the utilization of plastic products in the population. We found that low-dose microplastic exposure accelerated dopamine neuron degeneration and the onset of movement disorders in vivo, inducing a PD-like neuronal pathology through its effects on the intestinal mucosal barrier, immune barrier, and microbial barrier. Notably, non-penetrating microplastics facilitated neuroinflammation by triggering excessive reactive oxygen species production and a sustained UPR^mt. Furthermore, our population survey demonstrated that inappropriate use was a major source of microplastics in the gastrointestinal tract. The high use of disposable plastic tableware, especially in those with definite microplastic exposure, was also associated with intestinal inflammatory symptoms. As a novel pollutant, microplastic exposure in vivo undoubtedly executes an important role in the degeneration of dopamine neurons, regardless of barrier penetration, which is a non-independent risk factor that cannot be ignored in the pathogenesis of PD.