Nanomaterials are used in medical, industrial, and consumer settings, but their effects on the nervous system remain difficult to interpret because different materials vary widely in composition, size, surface chemistry, and exposure behavior. Epigenetic regulation provides a possible link between these material-dependent exposures and changes in neural function. This review critically discusses evidence that nanomaterials may alter DNA methylation, histone modifications, noncoding RNA expression, RNA modifications, chromatin organization, and genomic imprinting in models relevant to neurotoxicity. Rather than considering nanomaterials as a uniform class, we emphasize how epigenetic responses differ according to material properties, exposure route, dose, exposure duration, developmental stage, and biological model. These changes have been associated with oxidative stress, neuroinflammation, glial activation, blood-brain barrier dysfunction, impaired synaptic signaling, neuronal injury, and altered neurodevelopment. Evidence from gut-brain, lung-brain, and liver-brain interactions further suggests that peripheral tissues may shape the timing and regional pattern of nanomaterial-related neural injury. However, many reported epigenetic changes remain correlative, and findings from nonneural cells or high-dose short-term exposure models should not be directly generalized to the central nervous system. Future work should improve exposure characterization, distinguish direct neural evidence from indirect mechanistic evidence, and test whether specific epigenetic changes have predictive or causal value in nanomaterial-induced neurotoxicity through longitudinal, dose-responsive, and functional perturbation studies.
Liu et al. (Thu,) studied this question.