Research in genetic and molecular mechanisms underlying neuropathology has revealed significant insights into various conditions, particularly meningiomas and neurodegenerative disorders. A study identified chromosomal alterations, specifically loss of chromosome 1p and gain of 1q, which could enhance the grading of meningiomas, suggesting that patients with WHO grade 1 tumors exhibiting 1p loss have outcomes comparable to those with grade 2 tumors (ref: Landry doi.org/10.1001/jamaoncol.2025.0329/). Another investigation characterized BAP1-altered meningiomas as a distinct and aggressive CNS tumor subtype, marked by recurrent loss of chromosome 3p21 and dysregulation of Polycomb repressive complex target genes, emphasizing the need for tailored therapeutic approaches (ref: Sievers doi.org/10.1093/neuonc/). In the realm of neurodegenerative diseases, a comprehensive genome-wide association study involving 985 patients confirmed UNC13A as a major risk factor for frontotemporal lobar degeneration with TDP-43 inclusions, while also identifying TNIP1 as a novel risk factor, thus expanding the understanding of genetic predispositions in FTLD-TDP (ref: Pottier doi.org/10.1038/s41467-025-59216-0/). Furthermore, the integration of transcriptome-wide association studies with functional validation has pinpointed 123 candidate genes associated with Alzheimer’s disease risk loci, many of which correlate with neuropathological changes in human AD brains (ref: Stephens doi.org/10.1016/j.ajhg.2025.03.012/). Lastly, the interplay between sleep patterns and amyloid-beta pathology has been highlighted, indicating that disrupted sleep can exacerbate amyloid deposition, thereby linking circadian rhythms to neurodegenerative processes (ref: Turton doi.org/10.1016/j.bbadis.2025.167840/).

The immune response and neuroinflammation are critical areas of study in understanding various neurological disorders. Recent findings indicate that therapy-induced senescent glioblastoma cells can create a pro-cancer immune microenvironment through DDX58-mediated STAT1 signaling, which diminishes survival in animal models (ref: Wang doi.org/10.1093/neuonc/). Additionally, a study on a murine model of spastic paraplegia revealed that microglial activation and CD8+ T cell expansion precede neuronal loss, suggesting a significant role of the immune system in neurodegeneration (ref: Frolov doi.org/10.1084/jem.20232357/). In aging mice, the accumulation of monocyte-derived microglia has been linked to motor deficits, highlighting the impact of immune cell dynamics on neurological function (ref: Kim doi.org/10.1016/j.celrep.2025.115609/). Furthermore, targeting SARM1 has emerged as a promising neuroprotective strategy in viral encephalitis, underscoring the potential for immune modulation in treating neurotropic viral infections (ref: He doi.org/10.1186/s12974-025-03423-5/). Lastly, a study investigating post-resuscitation blood pressure management in a porcine model demonstrated that varying mean arterial pressure targets can influence cerebral perfusion and inflammatory responses, providing insights into optimizing neuroprotection following cardiac arrest (ref: García Bardon doi.org/10.1016/j.resplu.2025.100930/).

Neurodegenerative disorders and the search for reliable biomarkers have been focal points in recent research. A study on amyotrophic lateral sclerosis (ALS) highlighted the asymmetrical onset of motor symptoms, suggesting that the neurobiological mechanisms behind this lateralized progression remain poorly understood (ref: Yoganathan doi.org/10.1093/brain/). In the context of spinal cord diffuse midline glioma, cytarabine (Ara-C) was found to suppress tumor growth and enhance sensitivity to immune checkpoint blockade, indicating potential therapeutic avenues for H3 K27-altered tumors (ref: Pang doi.org/10.1126/sciadv.adu3956/). Additionally, the modulation of microRNA expression in response to amyloid-beta toxicity has been proposed as a step toward discovering biomarkers for Alzheimer's disease, emphasizing the role of miRNAs in neuronal health (ref: Keske doi.org/10.1007/s12035-025-04895-5/). The regulation of MCCC1 expression by a Parkinson's disease-associated variant has also been investigated, shedding light on genetic factors contributing to disease pathogenesis (ref: Sogabe doi.org/10.1038/s10038-025-01335-z/). Furthermore, the impact of post-resuscitation blood pressure management on cerebral perfusion and inflammation in a porcine model underscores the importance of optimizing care in neurodegenerative contexts (ref: García Bardon doi.org/10.1016/j.resplu.2025.100930/).

The field of tumor biology and treatment strategies has seen significant advancements, particularly concerning meningiomas and other CNS tumors. A study on TMEM106B overexpression in transgenic mice demonstrated that increased levels lead to lysosomal dysfunction, negatively impacting neuronal health and synaptic signaling (ref: Perneel doi.org/10.1186/s13024-025-00831-2/). Additionally, the evaluation of CDKN2A copy number status in meningiomas revealed pitfalls in current assessment methods, emphasizing the need for improved diagnostic accuracy in determining malignancy (ref: Zschernack doi.org/10.1007/s11060-025-05029-6/). The histological and molecular characterization of endolymphatic sac tumors has also provided insights into distinguishing these tumors from their primary differential diagnosis, choroid plexus papilloma, which is crucial for accurate diagnosis and treatment planning (ref: Friker doi.org/10.14670/HH-18-920/). Furthermore, the restoration of blood-brain barrier integrity following neurosurgical resection in drug-resistant epilepsy patients has been documented, highlighting the potential for surgical interventions to improve outcomes (ref: Behan doi.org/10.1016/j.yebeh.2025.110425/). Lastly, the association of NOR-1 overexpression with enhanced mitochondrial function and endurance in aged skeletal muscles suggests a novel angle for therapeutic strategies targeting muscle health in neurodegenerative contexts (ref: Paez doi.org/10.1096/fj.202500375R/).

Research into neuronal function and synaptic health has unveiled critical insights into the mechanisms underlying neurodegeneration and neuronal resilience. A study demonstrated that correcting dysregulated lipid metabolism in oligodendrocytes can normalize gene expression and prolong lifespan in poly-GA C9orf72 mice, suggesting that lipid homeostasis is vital for neuronal health (ref: Rezaei doi.org/10.1038/s41467-025-58634-4/). Another investigation revealed that elevated homocysteine levels enhance the excitability of cultured hippocampal neurons without altering the expression of voltage-gated ion channels, indicating a potential mechanism by which hyperhomocysteinemia contributes to neurological disorders (ref: Filipova doi.org/10.1186/s13041-025-01205-x/). The interactions between sleep-wake rhythms and amyloid-beta pathology have also been explored, with findings suggesting that disrupted sleep can exacerbate amyloid deposition, thereby linking circadian rhythms to synaptic health (ref: Turton doi.org/10.1016/j.bbadis.2025.167840/). Furthermore, the loss of NgBR was shown to cause neuronal damage through decreased acetylation of RFX1 and reduced FGF1 expression, highlighting the importance of genetic factors in maintaining neuronal integrity (ref: Hu doi.org/10.1007/s00018-025-05660-6/). Lastly, the association of phosphorylation status of ERK with genetic MAPK alterations in pediatric tumors underscores the complexity of signaling pathways in tumor biology and their implications for treatment (ref: Selt doi.org/10.1038/s41598-025-98514-x/).

Understanding the pathological mechanisms in neurodegeneration has been a focal point of recent studies, particularly in distinguishing atypical parkinsonian syndromes. Research has shown that cognitive and neuropsychiatric profiles can effectively differentiate these syndromes from Parkinson's disease, with specific deficits observed in executive function and visuospatial abilities (ref: Hu doi.org/10.1093/brain/). Additionally, the developmental deletion of amyloid precursor protein (APP) has been linked to impaired transcriptional and proteomic responses following brain injury, suggesting that APP plays a crucial role in brain repair mechanisms (ref: Lacovich doi.org/10.1002/alz.70093/). The molecular interplay of ISG15 and ISGylation has also been highlighted, with implications for neuroprotection and neurodegeneration across various neuropathies, including Alzheimer's and Parkinson's diseases (ref: Tecalco-Cruz doi.org/10.2174/0118715273378149250322050004/). Furthermore, a comparative evaluation of therapeutic modalities in CNS embryonal tumors with PLAGL amplification revealed significant heterogeneity in clinical outcomes, emphasizing the need for tailored treatment strategies (ref: Keck doi.org/10.1111/nan.70015/). Collectively, these studies underscore the complexity of neurodegenerative processes and the necessity for continued research into their underlying mechanisms.