Recent studies have highlighted the intricate relationship between genetic and epigenetic factors in various neuropathologies, particularly gliomas and Alzheimer's disease. Dejaegher et al. explored the role of DNA methylation in glioblastoma subclassification, revealing that distinct epigenetic groups correlate with immune cell infiltration and patient survival outcomes. Their analysis of 93 glioblastoma samples demonstrated that specific methylation patterns could serve as prognostic indicators, emphasizing the importance of molecular subclassification in tailoring therapeutic approaches (ref: Dejaegher doi.org/10.1093/neuonc/). Similarly, Sievers et al. identified a unique DNA methylation profile in a subset of pediatric thalamic gliomas, which frequently harbored alterations in the EGFR gene, underscoring the biological diversity within malignant astrocytic gliomas in children (ref: Sievers doi.org/10.1093/neuonc/). Furthermore, Suwala et al. reported a novel epigenetic group of IDH-mutant astrocytomas characterized by hereditary mismatch repair deficiency, which is associated with a poor prognosis, highlighting the need for genetic screening in treatment planning (ref: Suwala doi.org/10.1007/s00401-020-02243-6/). In the context of Alzheimer's disease, Hong et al. conducted a genome-wide association study that elucidated the genetic architecture of CSF biomarkers, providing insights into the underlying disease mechanisms and potential avenues for clinical prediction models (ref: Hong doi.org/10.1038/s41398-020-01074-z/). Karschnia et al. further contributed to this theme by demonstrating that the extent of MGMT promoter methylation in gliomas is significantly associated with other molecular markers and can provide additional prognostic information, particularly in IDH-wildtype astrocytomas (ref: Karschnia doi.org/10.1038/s41598-020-76312-x/). Collectively, these studies illustrate the critical role of genetic and epigenetic mechanisms in shaping the clinical behavior of neurological diseases and underscore the potential for personalized medicine based on molecular profiling.

The tumor microenvironment plays a pivotal role in the progression and treatment response of various brain tumors, as evidenced by recent research focusing on medulloblastoma and glioblastoma. Albert et al. utilized single-cell transcriptomics and biophysical methods to identify an extracellular vesicle-related gene expression signature that distinguishes high-risk medulloblastoma patients, revealing the complexity of intercellular communication within the tumor niche (ref: Albert doi.org/10.1093/neuonc/). In a complementary study, Tan et al. demonstrated that CSF1R inhibition effectively depletes tumor-associated macrophages in a mouse model of sonic hedgehog medulloblastoma, leading to reduced tumor progression. Their findings suggest that the immune microenvironment, particularly the role of tumor-associated macrophages, is crucial in mediating tumor behavior and could be targeted for therapeutic benefit (ref: Tan doi.org/10.1038/s41388-020-01536-0/). Zhai et al. further explored the interactions between glioma stem cells and immune cells during tumorigenesis, revealing shifts in these interactions that may contribute to glioblastoma's aggressive nature and limited immune response (ref: Zhai doi.org/10.3389/fimmu.2020.581209/). This body of work emphasizes the importance of understanding the tumor microenvironment and immune interactions in developing effective treatment strategies for brain tumors. Additionally, Sawant et al. investigated the role of thyroid hormone signaling in retinopathy of prematurity, highlighting the broader implications of molecular mechanisms in neurodevelopmental disorders and their potential impact on tumor biology (ref: Sawant doi.org/10.1167/iovs.61.13.36/).

The identification of biomarkers and imaging techniques for neurodegenerative diseases has gained significant attention, particularly in Alzheimer's disease and related disorders. Josephs et al. examined the contributions of TDP-43 and tau proteins to brain atrophy in Alzheimer's disease and primary age-related tauopathy, finding that TDP-43 is associated with accelerated brain atrophy rates, albeit at different time points in each condition (ref: Josephs doi.org/10.1093/brain/). Soleimani-Meigooni et al. conducted a study comparing 18F-flortaucipir PET imaging with post-mortem pathology, revealing that patients with non-Alzheimer tauopathies exhibited varying levels of tracer retention, which could inform differential diagnoses in clinical settings (ref: Soleimani-Meigooni doi.org/10.1093/brain/). Lesman-Segev et al. focused on the diagnostic accuracy of amyloid PET imaging, demonstrating its utility in distinguishing between Alzheimer's disease and non-Alzheimer patterns, thus enhancing diagnostic precision (ref: Lesman-Segev doi.org/10.1002/ana.25968/). Feng et al. contributed to the field by developing a novel methylation signature that predicts radiotherapy sensitivity in gliomas, which could serve as a valuable tool for personalized treatment approaches (ref: Feng doi.org/10.1038/s41598-020-77259-9/). Hierweger et al. explored the neuropathological features associated with cerebral ovine herpesvirus 2 infection in cattle, providing insights into the variability of neuropathological phenotypes across species (ref: Hierweger doi.org/10.1177/0300985820970493/). Together, these studies underscore the importance of biomarkers and imaging in understanding neurodegenerative diseases and improving clinical outcomes.

Clinical outcomes and prognostic factors in brain tumors have been extensively studied, particularly in glioblastoma and related malignancies. Zhai et al. highlighted the interactions between glioma stem cells and immune cells, revealing that these dynamics significantly influence tumor progression and patient outcomes (ref: Zhai doi.org/10.3389/fimmu.2020.581209/). Karschnia et al. provided critical insights into the prognostic value of MGMT promoter methylation in WHO grade II gliomas, demonstrating that higher levels of methylation correlate with favorable outcomes, particularly in the absence of 1p19q co-deletion (ref: Karschnia doi.org/10.1038/s41598-020-76312-x/). Farrell et al. conducted a systematic review and evidence-based guidelines update on the management of newly diagnosed glioblastoma, recommending the use of 5-aminolevulinic acid to enhance tumor resection and suggesting the assessment of IDH1 mutation status as a predictor of survival (ref: Farrell doi.org/10.1007/s11060-020-03607-4/). Petropoulou et al. explored the role of Lipocalin-2 as an anorexigenic signal in primates, providing a novel perspective on metabolic factors that may influence clinical outcomes in brain tumor patients (ref: Petropoulou doi.org/10.7554/eLife.58949/). Nann et al. characterized the genetic heterogeneity of follicular lymphoma, emphasizing the need for personalized approaches in treatment based on genetic profiling (ref: Nann doi.org/10.1182/bloodadvances.2020002944/). Collectively, these studies highlight the multifaceted nature of clinical outcomes in brain tumors and the critical role of molecular and genetic factors in guiding treatment strategies.

Recent research has shed light on the neuropathological features associated with infectious and inflammatory diseases, particularly in the context of COVID-19 and genetic neuropathies. Kirschenbaum et al. reported significant neuropathological findings in COVID-19 patients, including intracerebral endotheliitis and microbleeds, which may contribute to the neurological symptoms observed in these individuals (ref: Kirschenbaum doi.org/10.1111/nan.12677/). Laimer et al. investigated the use of hyperspectral imaging to differentiate between amalgam tattoos and other pigmented intraoral lesions, demonstrating the potential of advanced imaging techniques in diagnosing complex conditions (ref: Laimer doi.org/10.1002/jbio.202000424/). Chen et al. expanded the understanding of PLEKHG5-associated neuropathies by identifying novel pathogenic variants linked to Charcot-Marie-Tooth disease and spinal muscular atrophy, highlighting the genetic underpinnings of these conditions (ref: Chen doi.org/10.1111/ene.14649/). Russell et al. focused on social cognition impairments in familial frontotemporal dementia, revealing early changes in emotion processing and theory of mind abilities that precede clinical symptoms (ref: Russell doi.org/10.1016/j.cortex.2020.08.023/). Hierweger et al. characterized the neuropathological phenotype of malignant catarrhal fever in cattle, providing insights into cross-species infections and their neurological implications (ref: Hierweger doi.org/10.1177/0300985820970493/). Together, these studies underscore the importance of understanding the neuropathological features associated with infectious and inflammatory diseases to inform clinical management and therapeutic strategies.

The exploration of molecular mechanisms underlying neurodevelopmental disorders has revealed critical insights into their pathogenesis and potential therapeutic targets. Dewan et al. investigated the role of pathogenic huntingtin repeat expansions in frontotemporal dementia and amyotrophic lateral sclerosis, finding that such expansions were present in a small subset of patients, suggesting a complex genetic landscape in these disorders (ref: Dewan doi.org/10.1016/j.neuron.2020.11.005/). Hill et al. conducted a multicenter cohort study examining the time, pattern, and outcomes of medulloblastoma relapse, linking clinical and molecular characteristics at diagnosis to subsequent disease progression, which could inform management strategies (ref: Hill doi.org/10.1016/S2352-4642(20)30246-7/). Yao et al. developed the Alzheimer's Disease Cognitive Resilience Score, providing a novel framework for quantifying cognitive resilience in the presence of Alzheimer's pathology, which may have implications for understanding resilience mechanisms in neurodevelopmental disorders (ref: Yao doi.org/10.1371/journal.pone.0241707/). Kim et al. examined structural brain changes associated with recent suicidal behavior, identifying specific cortical and subcortical alterations that may inform risk assessment and intervention strategies (ref: Kim doi.org/10.1016/j.psychresns.2020.111216/). Huettl et al. highlighted the diagnostic challenges posed by cytokeratin expression in plasmablastic lymphoma, emphasizing the need for careful histopathological evaluation in neurodevelopmental contexts (ref: Huettl doi.org/10.1111/his.14300/). Collectively, these studies illustrate the multifaceted molecular mechanisms involved in neurodevelopmental disorders and their implications for diagnosis and treatment.

The identification of therapeutic targets and treatment strategies for neurological disorders has been a focal point of recent research, with promising findings across various studies. Broekaart et al. investigated the matrix metalloproteinase inhibitor IPR-179, demonstrating its antiseizure and antiepileptogenic effects in both rapid-kindling and kainic acid models, suggesting its potential as a therapeutic agent for epilepsy (ref: Broekaart doi.org/10.1172/JCI138332/). Charmsaz et al. identified the ADAM22/LGI1 complex as a novel actionable target for breast cancer brain metastasis, validating its role through global transcriptomic analysis and in vivo models, which may lead to new treatment avenues for metastatic disease (ref: Charmsaz doi.org/10.1186/s12916-020-01806-4/). Sawant et al. explored the role of thyroid hormone signaling in retinopathy of prematurity, providing insights into the molecular mechanisms that could be targeted for therapeutic intervention in this condition (ref: Sawant doi.org/10.1167/iovs.61.13.36/). Velázquez Vega et al. emphasized the importance of neuropathology in managing newly diagnosed glioblastoma, recommending molecular-genetic testing to guide treatment decisions and improve patient outcomes (ref: Velázquez Vega doi.org/10.1007/s11060-020-03616-3/). Bohnert et al. highlighted the potential of metabolomics in postmortem cerebrospinal fluid diagnostics, suggesting that metabolic profiling could enhance our understanding of central nervous system-related pathological processes and inform therapeutic strategies (ref: Bohnert doi.org/10.1007/s00414-020-02462-2/). Together, these studies underscore the importance of identifying and validating therapeutic targets to improve treatment outcomes in neurological disorders.