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From Heatwaves to Brainwaves: Climate-Driven Microplastics Promote Epstein–Barr Virus Reactivation and Female-Biased Risk for Alzheimer’s Disease and Multiple Sclerosis
Summary
Scientists used computer models to study how tiny plastic particles (microplastics) from climate change might work together with a common virus called Epstein-Barr to increase the risk of brain diseases like Alzheimer's and multiple sclerosis. They found that microplastics contain chemicals that act like hormones in the body and may help reactivate this virus, potentially explaining why women have higher rates of these diseases. While this research needs to be tested in real people, it suggests that plastic pollution could be another factor affecting our brain health.
Abstract Background Climate change accelerates plastic degradation, increasing human exposure to microplastics and their associated endocrine-disrupting additives, thereby reshaping the chemical exposome. Many of these compounds, including bisphenols and phthalates, act as xenoestrogens capable of perturbing hormonal, immune, and oxidative stress pathways within the internal biological exposome. Persistent viral infections such as Epstein–Barr virus (EBV), which dynamically interact with immune and redox regulation, further shape the biological exposome. We hypothesized that climate-associated microplastic compounds may converge with EBV-related molecular networks within the exposome that are implicated in Alzheimer’s disease (AD) and multiple sclerosis (MS). Methods We developed a computational exposome modelling framework integrating network toxicology and systems bioinformatics to map known and predicted human targets of microplastic-derived compounds with EBV–host protein–protein interactions and AD- and MS-associated proteins. Integrated interaction networks were constructed, and pathway enrichment analyses were performed to identify molecular points of convergence across environmental, viral, and disease-associated networks. Results Microplastic-responsive targets were enriched in immune, oxidative stress, and endocrine signalling pathways within both AD and MS networks and overlapped extensively with viral infection–associated pathways, including EBV. EBV interfaced with a greater number of AD-associated proteins than MS-associated proteins, whereas immune-related pathways predominated in MS. A conserved set of 20 EBV–microplastic “dual-hit” host proteins was identified across both diseases. In AD, the dual-hit neighbourhood was enriched for neuronal, metabolic, and hormone-responsive pathways, including neurotrophin signalling, dopaminergic synapse, estrogen signalling, apoptosis, and cellular senescence. In MS, enrichment was dominated by innate and adaptive immune pathways, including Toll-like receptor, IL-17, TNF, and JAK–STAT signalling. Estrogen signalling emerged as an AD-specific enriched pathway, while progesterone-mediated oocyte maturation was enriched in both diseases. Conclusions These findings provide systems-level, hypothesis-generating evidence that climate-associated microplastic exposure may intersect with endocrine and EBV-related host pathways relevant to neurodegenerative and autoimmune disease vulnerability. Although experimental validation is required, this exposome-based framework highlights molecular convergence points through which environmental and viral factors may jointly modulate disease-relevant biological networks, with potential implications for sex-related differences in susceptibility.