Blood–Brain Barrier Disruption by Microplastics and Nanoplastics: Implications for Neurodegeneration

This review critically examines current evidence regarding the ability of microplastics and nanoplastics (MNPs) to interact with and traverse the blood–brain barrier (BBB), their neurotoxic effects, and their potential relevance to pathways associated with neurodegenerative diseases. Experimental evidence indicates that MNPs can reach neural tissues and disrupt BBB integrity, with transport and biological effects influenced by particle size, shape, surface properties, and chemical composition. In vitro and animal studies demonstrate that MNP exposure can induce oxidative stress, mitochondrial dysfunction, neuroinflammation, BBB impairment, and altered proteostasis. These responses overlap with mechanisms implicated in Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). Emerging human studies have also detected plastic particles in postmortem brain tissue and cerebrospinal fluid, raising concerns regarding potential CNS exposure. However, human evidence remains limited, and the observed molecular and cellular responses are not specific to MNP exposure or individual neurodegenerative diseases. Current evidence supports the biological plausibility of MNP-induced neurotoxicity but does not establish a causal relationship between MNP exposure and human neurodegenerative disease. Oxidative stress, inflammation, mitochondrial dysfunction and impaired proteostasis are shared responses across numerous environmental toxicants and pathological conditions. Therefore, associations between MNP exposure and AD, PD or ALS should be interpreted cautiously. Standardized and contamination-controlled analytical methods, environmentally relevant exposure models, and longitudinal epidemiological studies are required to determine whether chronic MNP exposure represents an independent neurological risk factor or modifies existing vulnerability to neurodegenerative disease.