Recent studies have significantly advanced our understanding of the molecular mechanisms underlying brain tumors, particularly gliomas and medulloblastomas. A multi-cohort study by Negm explored the landscape of primary mismatch repair deficient gliomas in children, adolescents, and young adults, revealing that MMRD is a critical pan-cancer mechanism that presents unique biological and therapeutic opportunities (ref: Negm doi.org/10.1016/S1470-2045(24)00640-5/). In another study, Yin developed arrayed CRISPR libraries for genome-wide gene activation, deletion, and silencing, which could facilitate the identification of novel therapeutic targets in gliomas (ref: Yin doi.org/10.1038/s41551-024-01278-4/). Furthermore, Filser's research on nanopore sequencing demonstrated its efficacy in classifying medulloblastomas by providing clinically relevant methylation and copy number profiles, thus establishing a new standard for tumor classification (ref: Filser doi.org/10.1093/neuonc/). McFaline-Figueroa's investigation into neoadjuvant anti-PD1 immunotherapy in recurrent glioblastoma identified a unique cell cycle gene signature associated with improved survival, highlighting the potential of immunotherapy in this context (ref: McFaline-Figueroa doi.org/10.1038/s41467-024-54326-7/). Additionally, Boßelmann's analysis of 1386 epileptogenic brain lesions revealed significant associations with DYRK1A and EGFR, suggesting genetic underpinnings that could inform treatment strategies (ref: Boßelmann doi.org/10.1038/s41467-024-54911-w/). Karimian-Jazi's work on APTw CEST MRI provided insights into differentiating glioma recurrence from pseudoprogression, establishing a new imaging biomarker for neuro-oncology (ref: Karimian-Jazi doi.org/10.1097/RLI.0000000000001145/). Lastly, Zhu's study on adult primary leptomeningeal gliomatosis characterized its molecular profile, aligning it with glioblastoma, IDH-wildtype, and underscoring the need for targeted therapeutic approaches (ref: Zhu doi.org/10.1111/bpa.13326/).

The exploration of neurodegenerative disease pathology has unveiled critical insights into the molecular and genetic factors contributing to conditions such as Alzheimer's disease and amyotrophic lateral sclerosis (ALS). Schrempel's study identified isoAsp7-Aβ as a significant variant in Alzheimer's disease and other dementias, suggesting that specific post-translational modifications of Aβ may characterize different dementia types (ref: Schrempel doi.org/10.1007/s00401-024-02824-9/). Hickey's research highlighted the role of UBE3C and NRF1-dependent proteasomal pathways in controlling protein aggregate turnover, emphasizing the importance of proteostasis in neurodegenerative diseases (ref: Hickey doi.org/10.1073/pnas.2417390121/). In a comprehensive X-chromosome-wide association study, Le Borgne examined genetic factors associated with Alzheimer's disease, revealing significant insights into the genetic landscape of the disease (ref: Le Borgne doi.org/10.1038/s41380-024-02838-5/). Gigliucci's longitudinal imaging study in a mouse model of Charlevoix-Saguenay Ataxia provided valuable biomarkers for disease progression, linking retinal nerve fiber layer thickening to clinical outcomes (ref: Gigliucci doi.org/10.1002/ana.27146/). In a novel approach, Liao's study demonstrated that exogenous Neurexin-1 could induce neuron-like differentiation in glioma cells, presenting a potential therapeutic strategy for improving glioma prognosis (ref: Liao doi.org/10.1016/j.canlet.2024.217387/). Zimmermann's neuropathological examination of HTT repeat expansions in FTD/ALS found no significant correlation, challenging previous assumptions about their role in disease pathology (ref: Zimmermann doi.org/10.1007/s00415-024-12822-2/). Lastly, Zhu's investigation into isoaspartate formation in CRMP2 highlighted its implications for epilepsy and cognitive decline, suggesting that protein repair mechanisms are crucial in maintaining neuronal health (ref: Zhu doi.org/10.1007/s00726-024-03435-0/).

Neuroinflammation and immune responses play pivotal roles in various neurological disorders, as evidenced by recent studies elucidating the cellular and molecular mechanisms involved. Amann's research identified extrasinusoidal macrophages as a distinct subset of dural macrophages, contributing to our understanding of the immune landscape in the central nervous system (ref: Amann doi.org/10.1126/sciimmunol.adh1129/). Ovesen's work on the Alzheimer's disease risk gene SORL1 revealed its role in promoting microglial receptiveness to pro-inflammatory stimuli, suggesting that genetic variations can influence neuroinflammatory responses (ref: Ovesen doi.org/10.1002/glia.24659/). Magliozzi's examination of choroid plexus inflammation in progressive multiple sclerosis highlighted significant immune infiltration, linking it to broader inflammatory processes within the brain (ref: Magliozzi doi.org/10.1111/bpa.13322/). Floris's study integrated RNA sequencing to demonstrate transcriptional overlaps between neuroinflammation and heroin exposure, providing insights into the behavioral ramifications of inflammatory pathways in opioid use disorder (ref: Floris doi.org/10.1038/s41398-024-03203-4/). Additionally, Thomas's protocol for a multidisciplinary study on pediatric myalgic encephalomyelitis/chronic fatigue syndrome aims to uncover biological markers associated with this debilitating condition, emphasizing the need for comprehensive investigations into neuroinflammatory processes in adolescents (ref: Thomas doi.org/10.1136/bmjopen-2024-089038/).

The role of genetic and epigenetic factors in neuropathology has garnered significant attention, with studies revealing their impact on disease progression and treatment outcomes. Bajrami Saipi's research on iASPP expression in acute myeloid leukemia identified high levels as an independent predictor of adverse clinical outcomes, underscoring the importance of apoptosis-regulating proteins in cancer (ref: Bajrami Saipi doi.org/10.1038/s41419-024-07190-8/). Liao's investigation into neuron-like lineage differentiation in glioma cells demonstrated that enhancing neuronal differentiation-related gene expression could improve prognosis, suggesting a potential therapeutic avenue (ref: Liao doi.org/10.1016/j.canlet.2024.217387/). Cakmak's analysis of DNA methylation in giant cell-enriched glioblastoma revealed accelerated epigenetic aging, linking it to the distinct histological features of this tumor variant (ref: Cakmak doi.org/10.1186/s13148-024-01793-w/). Wasilewski's study on TTF-1 negativity in lung adenocarcinoma brain metastases found significant associations with larger tumor volumes and worse survival outcomes, indicating the prognostic value of molecular markers in metastatic disease (ref: Wasilewski doi.org/10.1007/s11060-024-04885-y/). Engertsberger's research on spinal ependymomas highlighted the prognostic impact of molecular classification, providing insights into the risk of disease progression in pediatric patients (ref: Engertsberger doi.org/10.1093/noajnl/).

The integration of clinical applications and biomarkers in neuro-oncology has advanced significantly, with studies focusing on prognostic subgrouping and imaging techniques. Akbari's multicenter study utilized machine learning to develop a prognostic subgrouping system for glioblastoma, stratifying patients into favorable, intermediate, and poor prognostic groups based on clinical data and molecular measures (ref: Akbari doi.org/10.1093/neuonc/). Karimian-Jazi's investigation into APTw CEST MRI provided a novel imaging biomarker for differentiating glioma recurrence from pseudoprogression, enhancing monitoring capabilities in neuro-oncology (ref: Karimian-Jazi doi.org/10.1097/RLI.0000000000001145/). Schmidt's research demonstrated that tonabersat could enhance temozolomide-mediated cytotoxicity in glioblastoma by disrupting intercellular connectivity, highlighting the potential for combination therapies (ref: Schmidt doi.org/10.1002/1878-0261.13786/). Oon's characterization of nodal gamma-delta T-cell lymphoma provided clinicopathological and molecular insights, contributing to the understanding of rare lymphoid malignancies (ref: Oon doi.org/10.1016/j.modpat.2024.100685/). Hiya's analysis of the National Alzheimer's Coordinating Center dataset revealed the clinical-pathological correlations of isolated and mixed neurodegenerative processes, emphasizing the complexity of dementia pathology (ref: Hiya doi.org/10.1093/jnen/).

Technological advances in neuro-oncology have revolutionized the field, particularly in the areas of gene editing and imaging techniques. Htet's study on the fluid mechanics of luminal transport in the endoplasmic reticulum provided insights into cellular processes that may influence neuro-pathologies, emphasizing the importance of understanding cellular dynamics (ref: Htet doi.org/10.7554/eLife.93518/). Yin's development of arrayed CRISPR libraries for genome-wide gene perturbation has expanded the capabilities of gene editing, allowing for comprehensive studies of human protein-coding genes (ref: Yin doi.org/10.1038/s41551-024-01278-4/). Meißner's assessment of artificial intelligence-based tumor classification using stimulated Raman histology demonstrated high image quality and reliability, paving the way for improved diagnostic techniques in neuro-oncology (ref: Meißner doi.org/10.3390/diagnostics14232701/). Chaturvedi's prospective observational study on pediatric diffuse intrinsic pontine gliomas highlighted the significance of clinical, radiological, and molecular features in understanding this aggressive tumor type (ref: Chaturvedi doi.org/10.1007/s00381-024-06730-z/).

Research in pediatric neuropathology has focused on understanding the unique characteristics and challenges associated with brain tumors in children and adolescents. Negm's study on primary mismatch repair deficient gliomas revealed critical insights into the biology and therapeutic opportunities for this patient population, emphasizing the need for tailored treatment approaches (ref: Negm doi.org/10.1016/S1470-2045(24)00640-5/). Merk's functional screening of atypical teratoid rhabdoid tumors identified genetic dependencies and diverging cell cycle control mechanisms, highlighting the urgent need for novel therapeutic strategies in this high-grade pediatric brain tumor (ref: Merk doi.org/10.1186/s13059-024-03438-w/). Filser's evaluation of nanopore sequencing for medulloblastoma classification demonstrated its potential to provide clinically relevant methylation and copy number profiles, establishing a new standard for tumor classification in pediatric patients (ref: Filser doi.org/10.1093/neuonc/). Bui's retrospective study on muscle biopsies in neonates and infants underscored the importance of morphological analyses in establishing precise molecular diagnoses for neuromuscular disorders, emphasizing the need for comprehensive diagnostic approaches in this vulnerable population (ref: Bui doi.org/10.1186/s40478-024-01882-0/).