Summary:
Microplastics are now widely distributed in the environment, with exposure to humans occurring through ingestion, inhalation, and, to a lesser extent, skin contact. This study is a narrative review looking at what quantity of microplastics humans ingest annually, and whether most are excreted. The review discusses that a small proportion can persist in the body, raising concerns about potential long-term health effects. Microplastics have been detected in food, human tissues, and remote environments, indicating widespread exposure. This study also describes how microplastics can enter the bloodstream and cross the blood-brain barrier, allowing them to reach the central nervous system. Their ability to penetrate biological barriers depends on factors such as particle size and surface properties. Once in the brain, microplastics may disrupt cellular processes by inducing oxidative stress, inflammation and mitochondrial dysfunction. These effects can lead to neuronal damage and compromised blood-brain barrier integrity. The study further suggests that these mechanisms may contribute to the development and progression of neurodegenerative diseases, particularly Alzheimer’s disease and Parkinson’s disease. In Alzheimer’s disease, microplastics may promote abnormal protein accumulation, which is a key feature of the condition. In Parkinson’s disease, they may contribute to the loss of dopaminergic neurons. Both conditions involve overlapping pathways such as oxidative stress, neuroinflammation, and mitochondrial dysfunction. This study highlights that neurodegenerative diseases are highly prevalent and represent a significant global health burden, particularly in ageing populations. Although there is increasing evidence linking microplastic exposure to neurological effects, the underlying mechanisms are not fully understood. Overall, this study suggests that microplastics may contribute to neurotoxicity through multiple biological pathways and emphasises the need for further research to clarify their role in human disease.
Abstract:
The widespread presence of microplastics (MPs) in the environment has raised significant concerns about their potential impact on human health. As of 2023, the Ocean Conservancy estimates that adults may ingest up to 121,000 MPs annually. While the majority of these particles are cleared from the body, a small fraction can persist, as MPs are non-biodegradable and resist breakdown, posing long-term health risks that remain poorly understood. This review explores the emerging link between MP exposure and the development of neurodegenerative diseases, particularly Alzheimer’s disease (AD) and Parkinson’s disease [1]. MPs appear capable of triggering neurotoxic pathways, including activation of resident immune cells in the brain, oxidative stress, blood–brain barrier (BBB) disruption, mitochondrial dysfunction, and neuronal damage, which may contribute to neuroinflammation and disease progression. Specifically, six MP-related mechanistic pathways associated with AD were identified: BBB disruption, chronic inflammation, oxidative stress and ROS generation, mitochondrial dysfunction, impaired autophagy and proteostasis, and epigenetic alterations. Similarly, six pathways were implicated in PD: BBB disruption, oxidative stress in dopaminergic neurons, mitochondrial dysfunction, microglial-driven neuroinflammation, α-synuclein aggregation, and gut–brain axis [2] disruption. Ultimately, our findings underscore the urgent need for further research into the neurological consequences of chronic MP exposure in humans and highlight the importance of strengthening global policies to curb plastic pollution and mitigate its long-term health risks.
Article Publication Date: 18/11/2025
DOI: 10.1007/s11010-025-05428-3
