Neurodegenerative diseases represent a significant global health burden, characterized by progressive loss of neuronal function and structure. While traditionally viewed as primarily neuronal disorders, recent research has highlighted the crucial roles of neuroglia-astrocytes, microglia, and oligodendrocytes in the pathogenesis and progression of these diseases. This review explores the dual nature of glial cells in neurodegenerative processes, focusing on their protective and potentially harmful functions in Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and other neurodegenerative disorders. We examine the complex interactions between different glial cell types and neurons, highlighting recent discoveries in glial-neuronal metabolic coupling, neuroinflammation, and protein aggregation. Advanced technologies, such as single-cell RNA sequencing and spatial transcriptomics, have revealed unprecedented glial heterogeneity and disease-specific glial states, reshaping our understanding of these cells’ roles in health and disease. The review also discusses emerging concepts in neuroglial research, including the role of extracellular vesicles in disease propagation, epigenetic regulation of glial function, and the application of artificial intelligence in glial biology. Finally, we explore the therapeutic implications of targeting glia in neurodegenerative diseases, addressing both the promising avenues and challenges in developing glial-focused interventions. By integrating recent advances in neuroglial research, this review provides a comprehensive overview of the field and highlights future directions for research and therapeutic development. Understanding the complex roles of neuroglia in neurodegenerative diseases is crucial for developing more effective treatments and ultimately improving patient outcomes.

Metabolic disorders, including diabetes, obesity, and chronic kidney disease (CKD), remain leading contributors to global morbidity and mortality. These conditions are intricately associated with oxidative stress and inflammation, which not only drive their pathophysiology but also exacerbate complications. Oxidative stress results from an imbalance between the production of reactive oxygen species (ROS) and the body's capacity to detoxify them, while inflammation involves a chronic immune response that contributes to tissue damage and metabolic dysfunction.The articles highlighted in this editorial present a comprehensive overview of recent advancements in elucidating the underlying mechanisms, identifying potential biomarkers, and developing therapeutic interventions that target oxidative stress and inflammation in metabolic disorders.The interplay between oxidative stress and inflammation plays a crucial role in the pathogenesis of metabolic disorders. At the cellular level, ROS are not merely byproducts of metabolism but also function as potent signaling molecules capable of inducing oxidative damage to proteins, lipids, and DNA. Songtao et al. investigated the role of claudin-2 (CLDN2), a tight junction protein, as a novel biomarker for prediabetes, highlighting its potential for early diagnosis [1].Their findings indicate that elevated CLDN2 levels are associated with impaired glucose tolerance and inflammation, providing critical insights into prediabetic conditions.In diabetic retinopathy (DR), Peng et al. highlighted the protective role of DJ-1, a multifunctional protein, in mitigating retinal ganglion cell damage under high-glucose conditions [2]. Their study demonstrated that DJ-1 preserves mitochondrial function and attenuates ROS generation, emphasizing the critical role of mitochondrial homeostasis in diabetic complications. These findings elucidate the molecular pathways linking oxidative stress to tissue damage and pave the way for targeted therapies aimed at preserving cellular integrity.Biomarkers play a crucial role in the identification, monitoring, and management of metabolic disorders. In this context, Songtao et al. identified CLDN2 as a potent biomarker and a valuable tool for early detection of prediabetes [1]. This is particularly significant given that prediabetes often progresses asymptomatically and can lead to serious complications if left untreated.Another promising diagnostic strategy involves the oxidative balance score (OBS), which quantifies the balance between dietary and lifestyle-derived antioxidants and pro-oxidants. Wen et al. demonstrated a significant inverse relationship between OBS and CKD risk using NHANES data, highlighting that higher antioxidant intake confers protection against CKD progression [3].Similarly, Yang et al. established a correlation between higher OBS and reduced serum uric acid levels, underscoring its potential role in hyperuricemia management [4]. These findings emphasize the need for holistic diagnostic tools that integrate oxidative stress dynamics, providing a more comprehensive approach to assessing and mitigating metabolic disorders.The review by Drygała et al. presents compelling evidence on the metabolic benefits of β-blockers, particularly third-generation agents such as nebivolol and carvedilol [5]. While traditionally employed in the management of cardiovascular disease (CVD), these agents exhibit antiinflammatory and antioxidant properties that extend beyond their primary pharmacological roles.Nebivolol enhances nitric oxide (NO) bioavailability, thereby reducing oxidative stress and improving endothelial function. Meanwhile, carvedilol modulates inflammatory pathways via the Nrf2/ARE signaling cascade, contributing to cellular protection against oxidative damage.Beyond their cardiovascular benefits, these agents also demonstrate potential in modulating insulin resistance and glucose metabolism. Nebivolol, owing to its vasodilatory properties, enhances skeletal muscle perfusion, thereby promoting glucose uptake. Similarly, carvedilol has been shown to exert favorable effects on insulin sensitivity and lipid profiles, making these β-blockers particularly beneficial for individuals with metabolic syndrome or type 2 diabetes.Targeting oxidative stress and inflammation has become a fundamental strategy in the treatment of metabolic disorders. Diphenyl diselenide (DPDS), investigated by Wang et al., exemplifies a promising therapeutic agent capable of modulating oxidative stress and gut microbiota in diabetic kidney disease (DKD) [6]. The study demonstrated that DPDS improves renal pathology by reducing ROS levels, enhancing antioxidant enzyme activity, and restoring gut microbial balance. Furthermore, the findings underscored the role of the Nrf2/Keap1 signaling pathway in mediating the protective effects of DPDS, reinforcing its potential as a therapeutic intervention for oxidative stress-related renal complications.Nutritional interventions represent another promising avenue for mitigating oxidative stress and inflammation. Hu et al. investigated Vernonia anthelmintica, a plant traditionally used in herbal medicine, and identified its flavonoid component, kaempferol, as a potent antioxidant [7].Kaempferol was shown to enhance antioxidant enzyme activity and suppress ROS generation in keratinocytes, demonstrating its potential therapeutic application in oxidative stress-related skin disorders. These findings highlight the synergistic interactions between natural bioactive compounds and key biochemical pathways, offering valuable insights into the development of antioxidant-based therapeutic strategies.Oxidative stress and inflammation pose significant risks in pediatric populations, where they contribute to long-term complications and disease progression. Lupu et al. investigated the impact of oxidative stress in pediatric diabetes, emphasizing its role in systemic decline, including damage to...

Background: Following the genome‐wide association studies (GWAS) discovery of microglia‐specific genes, particularly Trem‐2, SHIP‐1, and CD33, significantly associated with higher Alzheimer’s disease (AD) risk, the microglia TREM2 pathway has become central for regulating amyloid load, tissue damage, and limiting its spread. These discoveries have opened up the exciting possibility of therapeutic microglia TREM2 manipulation in AD. To date, however, several elements of TREM2 signaling remain unknown, ranging from the temporal activation pattern and receptor‐ligand binding to modulation of the brain microenvironment. This study aimed to investigate the consequences of reduced microglia Trem‐2 expression on oxidative stress, inflammatory response, and cognitive impairment. We hypothesized that a decrease in Trem‐2 expression would lead to an increase in oxidative stress markers, an up‐regulation of inflammatory cytokines, and a decline in cognitive functionMethod: We mimicked the neuroinflammatory milieu of AD by using LPS as a neuroinflammatory tool in vitro (BV2 microglia) and in vivo (C57BL6 mice).Result: We found that LPS‐induced reduction in Trem‐2 expression resulted in significantly higher levels of oxidative stress markers, including increased production of reactive oxygen species (increased DCFDA intensity), nitrite level, and reduced GSH content, both in vitro and in vivo. Likewise, we observed a significant increase in the level of tumor necrosis factor‐alpha (TNF‐α) in both the BV2 microglia and C57BL6 mice following LPS treatment. Furthermore, the MWM cognitive test revealed a decline in spatial memory and learning abilities in mice with decreased Trem‐2 expression compared to control mice.Conclusion: These results emphasize the importance of Trem‐2 in maintaining a healthy brain environment and suggest that targeting Trem‐2 could be a potential therapeutic strategy for neurodegenerative diseases associated with microglia dysfunction.