Nano- and microplastics (NMPs), with nanoplastics posing higher risks due to their smaller size and greater capacity for cellular and subcellular penetration, are being referred to as ubiquitous environmental neurotoxicants, due to their ability to pass through biological barriers, including the blood–brain barrier (BBB) and nasal olfactory epithelium, and to remain lodged in neural tissue. Upon uptake, such particles disturb neuronal homeostasis by multiple converging pathways, including oxidative stress, mitochondrial dysfunction, pathological protein aggregation, and chronic neuroinflammation, all closely involved with the molecular signatures of neurodegenerative disorders (Alzheimer’s, Parkinson’s, Amyotrophic Lateral Sclerosis—ALS). In addition to their neurotoxicity, recent findings suggest that NMPs could disturb synaptic communication and neuroplasticity, thereby compromising the brain’s capacity to recover from an injury, a trauma, or neurodegeneration, thus impacting the progression of the disease, our ability to treat it and eventually the efficacy of rehabilitation approaches. Despite these findings, our understanding remains hampered by analytical issues, the scarcity of standard detection methods, and a total lack of longitudinal studies in humans. This review combines multidisciplinary evidence on brain–plastic interactions and calls for accelerated advances in our ability to monitor bioaccumulation in humans, and to integrate neurotoxicology paradigms in the assessment of this underappreciated but growing threat to brain health.

Breast cancer (BC) is one of the most commonly diagnosed types of cancer in women. Oxidative stress may contribute to cancer etiology through several mechanisms. A large body of evidence indicates that physical activity (PA) has positive effects on different aspects of BC evolution, including mitigation of negative effects induced by medical treatment. With the aim to verify the capacity of PA to counteract negative effects of BC treatment on systemic redox homeostasis in postsurgery female BC patients, we have examined the modulation of circulating levels of oxidative stress and inflammation markers. Moreover, we evaluated the impacts on physical fitness and mental well-being by measuring functional parameters, body mass index, body composition, health-related quality of life (QoL), and fatigue. Our investigation revealed that PA was effective in maintaining plasma levels of superoxide dismutase (SOD) activity and tGSH, as well as peripheral blood mononuclear cells’ (PBMCs) mRNA levels of SOD1 and heat-shock protein 27. Moreover, we found a significant decrease in plasma interleukin-6 (≈0.57 ± 0.23-fold change, p < 0.05) and increases in both interleukin-10 (≈1.15 ± 0.35-fold change, p < 0.05) and PBMCs’ mRNA level of SOD2 (≈1.87 ± 0.36-fold change, p < 0.05). Finally, PA improves functional parameters (6 min walking test, ≈+6.50%, p < 0.01; Borg, ≈−58.18%, p < 0.01; sit-and-reach, ≈+250.00%, p < 0.01; scratch right, ≈−24.12%, and left, ≈−18.81%, p < 0.01) and body composition (free fat mass, ≈+2.80%, p < 0.05; fat mass, ≈−6.93%, p < 0.05) as well as the QoL (physical function, ≈+5.78%, p < 0.05) and fatigue (cognitive fatigue, ≈−60%, p < 0.05) parameters. These results suggest that a specific PA program not only is effective in improving functional and anthropometric parameters but may also activate cellular responses through a multitude of actions in postsurgery BC patients undergoing adjuvant therapy. These may include modulation of gene expression and protein activity and impacting several signaling pathways/biological activities involved in tumor-cell growth; metastasis; and inflammation, as well as moderating distress symptoms known to negatively affect QoL.

Micro- and nanoplastics (MNPs) are pervasive environmental contaminants with growing relevance for human health across the lifespan. Older adults may be especially vulnerable to their effects due to cumulative lifetime exposure, age-related physiological changes, and a higher burden of chronic disease. Adopting a One Health perspective, this review synthesizes current evidence on the sources, exposure pathways, and biological effects of MNPs, integrating findings from environmental, animal, and human studies with a specific focus on aging populations. Experimental studies consistently show that MNP exposure triggers oxidative stress, inflammation, mitochondrial dysfunction, and cellular senescence, mechanisms central to biological aging. These processes are linked to dysfunction of the cardiovascular, nervous, gastrointestinal, and immune systems, suggesting that MNPs may contribute to the development or progression of age-related diseases. Within the One Health framework, MNPs also act as carriers of chemical additives and environmental pollutants, potentially amplifying health risks through combined and cumulative exposures along food chains and ecosystems. Despite increasing mechanistic evidence, direct epidemiological data in older adults remain limited. This review highlights key knowledge gaps and emphasizes the need for integrative, longitudinal research to clarify the role of MNPs in aging and to inform public health and environmental policy.

Biological age, reflecting the cumulative damage in the body over a lifespan, is a dynamic measure more indicative of individual health than chronological age. Accelerated aging, when biological age surpasses chronological age, is implicated in poorer clinical outcomes, especially for breast cancer (BC) survivors undergoing treatments. This preliminary study investigates the impact of a 16-week online supervised physical activity (PA) intervention on biological age in post-surgery female BC patients. Telomere length was measured using qPCR, and the ELOVL2-based epigenetic clock was assessed via DNA methylation pyrosequencing of the ELOVL2 promoter region. Telomere length remained unchanged, but the ELOVL2 epigenetic clock indicated a significant decrease in biological age in the PA group, suggesting the potential of PA interventions to reverse accelerated aging processes in BC survivors. The exercise group showed improved cardiovascular fitness, highlighting PA’s health impact. Finally, the reduction in biological age, as measured by the ELOVL2 epigenetic clock, was significantly associated with improvements in cardiovascular fitness and handgrip strength, supporting improved recovery. Epigenetic clocks can potentially assess health status and recovery progress in BC patients, identifying at-risk individuals in clinical practice. This study provides potential and valuable insights into how PA benefits BC survivors’ health, supporting the immediate benefits of a 16-week exercise intervention in mitigating accelerated aging. The findings could suggest a holistic approach to improving the health and recovery of post-surgery BC patients.

Breast cancer (BC) continues to significantly impact women worldwide. Numerous studies show that physical activity (PA) significantly enhances the quality of life, aids recovery, and improves survival rates in BC patients. PA’s influence extends to altering DNA methylation patterns on both a global and gene-specific scale, potentially reverting abnormal DNA methylation, associated with carcinogenesis and various pathologies. This review consolidates the findings of the current literature, highlighting PA’s impact on DNA methylation in BC patients. Our systematic analysis indicates that PA may elevate global DNA methylation within tumour tissues. Furthermore, it appears to modify gene-specific promoter methylation across a wide spectrum of genes in various tissues. Through bioinformatic analysis, to investigate the functional enrichment of these affected genes, we identified a predominant enrichment in metabolic pathways, cell cycle regulation, cell cycle checkpoints, mitosis, cellular stress responses, and molecular functions governing diverse binding processes. The Human Protein Atlas corroborates this enrichment, indicating gene functionality across 266 tissues, notably within various breast tissues. This systematic review unveils PA’s capacity to systematically alter DNA methylation patterns across multiple tissues, particularly in BC patients. Emphasising its influence on crucial biological processes and functions, this alteration holds potential for restoring normal cellular functionality and the cell cycle. This reversal of cancer-associated patterns could potentially enhance recovery and improve survival outcomes.

Multiple Sclerosis (MS) is a neurological disorder that commonly begins in young adulthood and impacts central nervous system (CNS) through an autoimmune process. Pain is a frequent and heterogeneous symptom of this disease, but it is often overlooked and inadequately treated. Furthermore, among the most significant clinical manifestations, spasticity, present in 60-84% of MS patients, is not only a major disability factor but also contributes significantly to pain perception and worsening motor function.This systematic review and meta-analysis were conducted to evaluate the available evidence on the efficacy of Sativex® (Nabiximols), not only in pain control but also in the management of spasticity and disability caused by MS.A literature search was conducted on three main databases (PubMed, Scopus, and Web of Science), following the PRISMA guidelines, retrieving 1203 articles, of which 20 met the inclusion criteria and were selected for the systematic review and meta-analysis.Results showed a significant reduction in pain intensity, measured using the Numeric Rating Scale (NRS), after treatment with Sativex® (Standardized Mean Change [SMC]: -0.88, 95% CI -1.20 to -0.57, p < 0.0001). A significant reduction in spasticity severity was also observed (SMC: -1.29, 95% CI -1.63 to -0.94, p < 0.0001). In addition, a modest but statistically significant improvement in disability, assessed by Expanded Disability Status Scale (EDSS), was detected (SMC: -0.17, 95% CI -0.28 to -0.07, p = 0.0015). Overall, evidence suggests that Sativex may represent an effective therapeutic option for the management of pain and spasticity in patients with MS, with potential benefits for functional disability.