Moreover, the investigation into microglial dysfunction in the context of COVID-19 has revealed that systemic inflammation, particularly related to IL-1 and IL-6, is associated with neurovascular inflammation and focal neuropathologies, suggesting a critical role for microglia in the neurological manifestations of the disease (ref: Fekete doi.org/10.1038/s41593-025-01871-z/). The study of endosomal-lysosomal organellar assembly (ELYSA) structures in mouse oocytes has also shed light on the coordination of lysosomal degradation systems during embryogenesis, which may have implications for understanding cellular degradation processes in neuropathologies (ref: Satouh doi.org/10.7554/eLife.99358/). Collectively, these studies underscore the intricate molecular mechanisms at play in neuropathology, paving the way for novel therapeutic strategies.

Furthermore, the interplay between alpha-synuclein co-pathology and tau accumulation in Alzheimer's disease has been investigated, revealing that aggregated alpha-synuclein can exacerbate tau aggregation, potentially accelerating neurodegeneration and cognitive decline (ref: Franzmeier doi.org/10.1186/s13024-025-00822-3/). This highlights the necessity of considering alpha-synuclein in Alzheimer's research and treatment approaches. Additionally, testosterone signaling in microglia has been proposed as a factor contributing to sex-related differences in Alzheimer's disease prevalence, with GPRC6A being identified as a key mediator of this signaling pathway (ref: Du doi.org/10.1002/advs.202413375/). The role of interleukin-12 signaling in disrupting neuronal and oligodendrocyte homeostasis further underscores the complex relationship between microglial function and neuroinflammatory processes in neurodegenerative diseases (ref: Schneeberger doi.org/10.1038/s43587-025-00816-2/).

Moreover, a high-resolution proteomic analysis of clinical medulloblastoma samples has identified therapy-resistant subgroups, emphasizing the need for biology-driven risk stratification in clinical practice (ref: Delaidelli doi.org/10.1093/neuonc/). The study of extracellular vesicles carrying Tenascin-C has also emerged as a promising avenue for improving tumor-derived DNA analysis in glioblastoma patients, facilitating better monitoring of disease progression (ref: Salviano-Silva doi.org/10.1021/acsnano.4c13599/). These findings collectively highlight the importance of integrating molecular insights with therapeutic strategies to enhance patient outcomes in neuro-oncology.

The investigation of alpha-synuclein co-pathology has also underscored its role in accelerating tau accumulation in Alzheimer's disease, suggesting that genetic predispositions may influence the severity of neurodegenerative processes (ref: Franzmeier doi.org/10.1186/s13024-025-00822-3/). Furthermore, single-cell transcriptomics has identified the MIF-CD74 axis as a prominent factor in myasthenia gravis, illustrating how genetic and epigenetic mechanisms can drive autoimmune responses in the thymus (ref: Terroba-Navajas doi.org/10.1212/NXI.0000000000200384/). Lastly, the study of endosomal-lysosomal organellar assemblies in mouse oocytes has provided insights into the genetic regulation of cellular degradation processes, which may have broader implications for understanding neurodegenerative diseases (ref: Satouh doi.org/10.7554/eLife.99358/).

Additionally, the study of endosomal-lysosomal organellar assembly (ELYSA) structures in mouse oocytes has revealed important insights into lysosomal degradation systems, which are crucial for cellular homeostasis and may be disrupted in neurodegenerative conditions (ref: Satouh doi.org/10.7554/eLife.99358/). The identification of therapy-resistant subgroups in medulloblastoma through high-resolution proteomic analysis has also underscored the importance of understanding tumor biology in the context of neurodegeneration, as these insights can inform treatment strategies (ref: Delaidelli doi.org/10.1093/neuonc/). Collectively, these studies highlight the intricate interplay between genetic, epigenetic, and environmental factors in shaping neurodegenerative disease pathologies.

Moreover, studies have shown that telomere length and mitochondrial copy number in early pregnancy are associated with gestational diabetes mellitus and depressive symptoms, indicating that biological markers may predict adverse outcomes in maternal and child health (ref: Thirumoorthy doi.org/10.1016/j.psyneuen.2025.107431/). Additionally, elevated serum angiotensin II levels have been observed in children and adolescents with anxiety disorders, suggesting a potential biomarker for anxiety-related conditions (ref: Tanrıverdi doi.org/10.1016/j.psyneuen.2025.107430/). These findings collectively emphasize the need for a comprehensive understanding of the interplay between maternal factors, neurodevelopment, and behavioral outcomes in children.

Furthermore, the characterization of the T cell receptor landscape in childhood brain tumors has provided valuable information regarding tumor-infiltrating lymphocytes and their potential role in antitumor immunity, which could guide the development of immunotherapies (ref: Raphael doi.org/10.1126/scitranslmed.adp0675/). Additionally, the investigation of zipper-interacting protein kinase in traumatic brain injury has shed light on neuronal cell death mechanisms, suggesting that targeting this pathway may offer therapeutic opportunities (ref: Mei doi.org/10.1038/s41419-025-07474-7/). Collectively, these studies highlight the potential of neuroimaging and biomarker research to inform clinical practice and therapeutic strategies in neurology.