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Micro- and nanoplastics as environmental modifiers of neuroimmune dysfunction in Parkinson's disease
Original title: Micro- and nanoplastics as environmental modifiers of neuroimmune dysfunction in Parkinson’s disease
Summary
This review paper looks at how tiny plastic particles from pollution—called micro- and nanoplastics—might build up in the brain and trigger inflammation and immune system problems linked to Parkinson's disease. While scientists haven't yet proven that these plastics actually cause Parkinson's in humans, the research so far suggests they could act as a stress factor that makes the brain more vulnerable to damage, especially through effects on brain cells and the gut-brain connection. This matters because it highlights another reason to think about reducing everyday plastic exposure, even though more direct human studies are needed before drawing firm conclusions.
Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons and the aggregation of α -synuclein, with increasing evidence implicating environmental factors and neuroimmune dysfunction in its pathogenesis. Micro- and nanoplastics (MNPs), ubiquitous environmental pollutants generated from plastic degradation, have recently emerged as potential biological stressors capable of entering the human body and accumulating in sensitive tissues, including the brain. Due to their small size, environmental persistence, and capacity to carry toxic additives and environmental contaminants, these particles can induce oxidative stress, impair mitochondrial and lysosomal function, and activate both innate and adaptive immune responses. This review summarizes current evidence linking microplastic exposure to neuroinflammatory processes relevant to PD, with a particular focus on microglial activation, astrocyte reactivity, peripheral immune involvement, and dysfunction of the gut–brain axis. Although a direct causal relationship between MNPs and PD has yet to be established, and direct human epidemiological evidence linking MNP exposure to PD is currently absent, the immunotoxic and neuroinflammatory effects of these particles suggest that they may contribute to disease susceptibility and progression. Elucidating the interactions between MNPs and neuroimmune pathways may help refine current frameworks linking environmental exposure, neuroimmune dysfunction, and PD susceptibility.