Nanoplastics: An Emerging Threat to the Central Nervous System: From Blood-Brain Barrier Disruption to Neurotoxicity

Nanoplastics (NPs) have emerged as pervasive environmental contaminants with increasing concern regarding their potential effects on the central nervous system (CNS). Their nanoscale dimensions, high surface-to-volume ratio, and distinct physicochemical properties may facilitate biological interactions, cellular uptake, and translocation across physiological barriers, including the blood-brain barrier (BBB). This review synthesizes current evidence on the neurotoxic potential of NPs, with particular emphasis on their pathways of CNS entry, BBB disruption, cellular and molecular mechanisms of neurotoxicity, and potential neurological consequences. Available experimental evidence indicates that NPs can accumulate in brain tissue, with particle size, surface charge, polymer composition, shape, exposure duration, and surface characteristics influencing their distribution, persistence, and biological effects. BBB dysfunction appears to be an important component of NP-induced neurotoxicity, potentially facilitating further penetration and accumulation within neural tissue. Following CNS exposure, NPs have been associated with oxidative stress, mitochondrial impairment, microglial activation, neuroinflammation, altered neurotransmission, synaptic dysfunction, and neuronal injury. In addition, disruption of the gut-brain axis and impairment of glymphatic clearance may represent indirect mechanisms contributing to cognitive and neurobehavioral abnormalities. Experimental findings have also raised concerns regarding possible links between NP exposure and neurodegenerative processes, although mechanistic similarities with disorders such as Alzheimer's and Parkinson's disease should not be interpreted as evidence of causality in humans. Importantly, current evidence is predominantly derived from animal and in vitro models, while human studies remain limited. Considerable heterogeneity in NP characterization, exposure conditions, experimental models, and analytical methodologies further restricts direct comparison across studies. Future research should therefore prioritize standardized particle characterization, environmentally relevant exposure scenarios, improved analytical approaches for tissue quantification, and longitudinal human studies to establish the clinical relevance of NP-associated neurotoxicity and clarify their potential implications for neurological health.

کلیدواژه ها:

Nanoplastics ، Neurotoxicity ، Central Nervous System ، Blood-Brain Barrier ، Neuroinflammation ، Microglial Activation ، Oxidative Stress ، Mitochondrial Dysfunction ، Gut-Brain Axis