Acta Neuropathologica Communications最新文献

{"title":"Correction: Unraveling calcium dysregulation and autoimmunity in immune mediated rippling muscle disease.","authors":"Samir R Nath, Aneesha Dasgupta, Divyanshu Dubey, Eileen Kokesh, Grayson Beecher, Numrah Fadra, Teerin Liewluck, Sean Pittock, Jason D Doles, William Litchy, Margherita Milone","doi":"10.1186/s40478-025-01981-6","DOIUrl":"10.1186/s40478-025-01981-6","url":null,"abstract":"","PeriodicalId":6914,"journal":{"name":"Acta Neuropathologica Communications","volume":"13 1","pages":"66"},"PeriodicalIF":6.2,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11931796/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proximity proteomics reveals unique and shared pathological features between multiple system atrophy and Parkinson's disease.","authors":"Solji G Choi, Tyler R Tittle, Raj R Barot, Dakota J Betts, Johnie J Gallagher, Jeffrey H Kordower, Yaping Chu, Bryan A Killinger","doi":"10.1186/s40478-025-01958-5","DOIUrl":"10.1186/s40478-025-01958-5","url":null,"abstract":"<p><p>Synucleinopathies such as Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA) are neurodegenerative diseases with shared clinical and pathological features. Aggregates of alpha-synuclein (αsyn) phosphorylated at serine 129 (PSER129) are hallmarks of synucleinopathies, which, for PD/DLB, are found predominantly in neurons, whereas in MSA, aggregates are primarily found in oligodendroglia. It remains unclear whether the distinct pathological presentations of PD/DLB and MSA are manifestations of unique or shared pathological processes. Using the in-situ proximity labeling technique of biotinylation by antibody recognition (BAR), we compared aggregated αsyn-interactomes (BAR-PSER129) and total αsyn-interactomes (BAR-MJFR1) between MSA (n = 5) and PD/DLB (n = 10) in forebrain and midbrain structures. Comparison between MSA and PD/DLB-enriched proteins revealed 79 PD/DLB-differentially abundant proteins and only three MSA-differentially abundant proteins (CBR1, CRYAB, and GFAP). Pathway enrichment analysis revealed that vesicle/SNARE-associated pathways dominated PD/DLB interactions, whereas MSA was strongly enriched for metabolic/catabolic, iron, and cellular oxidant detoxification pathways. A subnetwork of cytosolic antioxidant enzymes called peroxiredoxins drove cellular detoxification pathway enrichment in MSA. A network of 26 proteins, including neuronal-specific proteins (e.g., SYNGR3) with HSPA8 at the core, was shared between MSA and DLB/PD. Extracellular exosome pathways were universally enriched regardless of the disease or BAR target protein. In conclusion, synucleinopathies have divergent and convergent αsyn-aggregate interactions, indicating unique and shared pathogenic mechanisms. MSA uniquely involves oxidant detoxification processes in glial cells, while vesicular processes in neurons dominate PD/DLB. Shared interactions, specifically SYNGR3, between MSA and PD/DLB suggest that neuronal axons are the origin of both diseases. In conclusion, we provide αsyn protein interaction maps for two distinct synucleinopathies.</p>","PeriodicalId":6914,"journal":{"name":"Acta Neuropathologica Communications","volume":"13 1","pages":"65"},"PeriodicalIF":6.2,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11931798/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143690802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Curative timed NK cell-based immunochemotherapy aborts brain tumour recurrence driven by mesenchymal glioma stem cells.","authors":"Brian Meehan, Lata Adnani, Xianbing Zhu, Nadim Tawil, Delphine Garnier, Ichiro Nakano, Sidong Huang, Janusz Rak","doi":"10.1186/s40478-025-01984-3","DOIUrl":"10.1186/s40478-025-01984-3","url":null,"abstract":"<p><p>High grade gliomas (HGG) are incurable brain cancers, where inevitable disease recurrence is driven by tumour-initiating glioma stem cells (GSCs). GSCs survive and expand in the brain after surgery, radiation and temozolomide (TMZ) chemotherapy, amidst weak immune and natural killer (NK) cell surveillance. The present study was designed to understand how to enhance the contribution of innate immunity to post TMZ disease control. Strikingly, molecular subtypes of HGG impacted the repertoire of NK cell sensitivity markers across human HGG transcriptomes, and in a panel of GSCs with either proneural (PN-GSC) or mesenchymal (MES-GSC) phenotypes. Indeed, only MES-GSCs (but not PN-GSCs) were enriched for NK cell ligands and sensitive to NK-mediated cytotoxicity in vitro. While NK cells alone had no effect on HGG progression in vivo, the post-chemotherapy (TMZ) recurrence of MES-GSC-driven xenografts was aborted by timed intracranial injection of live or irradiated NK (NK92MI) cells, resulting in long term survival of animals. This curative effect declined when NK cell administration was delayed relative to TMZ exposure pointing to limits of the immune control over resurging residual tumour stem cell populations that survived chemotherapy. Overall, these results suggest that chemotherapy-dependent tumour depopulation may create a unique window of opportunity for NK-mediated intervention with curative effects restricted to a subset of HGGs driven by mesenchymal brain tumour initiating cells.</p>","PeriodicalId":6914,"journal":{"name":"Acta Neuropathologica Communications","volume":"13 1","pages":"64"},"PeriodicalIF":6.2,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11927124/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143676779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chromogen-based double immunohistochemical detection of mitochondrial respiratory chain deficiencies in human brain tissue.","authors":"Tale L Bjerknes, Anna Rubiolo, Omnia Shadad, Ole-Bjørn Tysnes, Charalampos Tzoulis","doi":"10.1186/s40478-025-01980-7","DOIUrl":"10.1186/s40478-025-01980-7","url":null,"abstract":"<p><p>Studies of the mitochondrial respiratory chain (MRC) have given important insights into the pathology of mitochondrial and neurodegenerative disorders. Immunohistochemical methods for staining MRC complexes are particularly valuable for assessing quantitative changes in situ, especially in complex tissues with cellular heterogeneity, such as the brain. However, traditional approaches have notable limitations. Chromogen-based staining, while preserving tissue morphology, has been restricted to a single antigen per section, preventing co-assessment of MRC complexes and mitochondrial mass on the same section. Immunofluorescence, which allows multiplex staining of multiple targets, partially addresses this limitation but compromises tissue morphology and can be highly variable in postmortem brain samples. To address these challenges, we have established a dual-antigen, chromogen-based immunohistochemical method that allows simultaneous assessment of each MRC complex and the mitochondrial marker voltage-dependent anion channel 1 (VDAC1) on the same section. As proof of concept, we apply this method on brain tissue from patients with neurological disease caused by mutations in the mitochondrial DNA polymerase gamma (POLG). Our findings demonstrate that this approach is both reliable and robust. Moreover, this method enables more precise identification of MRC deficiencies in neurons and significantly reduces the amount of tissue required for analysis, a critical advantage when working with scarce human brain samples.</p>","PeriodicalId":6914,"journal":{"name":"Acta Neuropathologica Communications","volume":"13 1","pages":"63"},"PeriodicalIF":6.2,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924823/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatiotemporal perturbations of the plasminogen activation system in a rat model of acute organophosphate intoxication.","authors":"Thomas J Blackmon, Jeremy A MacMahon, Pedro N Bernardino, Ryan E Hogans, Mei-Yun Cheng, Joan Vu, Ruth Diana Lee, Naomi H Saito, Ana Cristina Grodzki, Donald A Bruun, Heike Wulff, Kevin D Woolard, Amy Brooks-Kayal, Danielle J Harvey, Fredric A Gorin, Pamela J Lein","doi":"10.1186/s40478-025-01979-0","DOIUrl":"10.1186/s40478-025-01979-0","url":null,"abstract":"<p><p>Neuroinflammation is widely posited to be a key pathogenic mechanism linking acute organophosphate (OP)-induced status epilepticus (SE) to persistent brain injury and abnormal electrical activity that contribute to epilepsy and cognitive impairment. The plasminogen activation system (PAS) promotes neuroinflammation in diverse neurological diseases but whether it is activated following acute OP intoxication has yet to be evaluated. To address this data gap, we characterized the spatiotemporal expression patterns of multiple components of the PAS in a rat model of acute intoxication with the OP, diisopropylfluorophosphate (DFP). Adult male Sprague Dawley rats administered DFP (4 mg/kg, sc), atropine sulfate (2 mg/kg, im) and 2-pralidoxime (25 mg/kg, im) went into SE that persisted for hours. One day after acute DFP-induced SE, plasmin activity and protein concentrations of plasminogen activator inhibitor-1 (PAI-1) in the plasma were increased, though not significantly. In contrast, acute DFP intoxication significantly increased brain levels of PAI-1, tissue-type plasminogen activator (tPA), urokinase plasminogen activator (uPA), and transcripts of TGF-β in a time- and region-dependent manner. In the cortex and hippocampus, quantification of PAI-1, tPA, and uPA by ELISA indicated significantly increased levels at 1 day post-exposure (DPE). PAI-1 and uPA returned to control values by 7 DPE while tPA protein remained elevated at 28 DPE. Immunohistochemistry detected elevated PAI-1 expression in the DFP brain up to 28 DPE. Co-localization of PAI-1 with biomarkers of neurons, microglia, and astrocytes demonstrated that PAI-1 localized predominantly to a subpopulation of astrocytes. Cytologically, PAI-1 localized to astrocytic end feet, but not adjacent neurovascular endothelium. Electron microscopy revealed neuronal metabolic stress and neurodegeneration with disruption of adjacent neurovascular units in the hippocampus post-DFP exposure. These data indicate that acute DFP intoxication altered PAS expression in the brain, with aberrant PAI-1 expression in a subset of reactive astrocyte populations.</p>","PeriodicalId":6914,"journal":{"name":"Acta Neuropathologica Communications","volume":"13 1","pages":"62"},"PeriodicalIF":6.2,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11917081/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143655786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic profiling of adult and pediatric gliomas reveals enriched glucose availability in pediatric gliomas and increased fatty acid oxidation in adult gliomas.","authors":"Vladislav O Sviderskiy, Varshini Vasudevaraja, Luiz Gustavo Dubois, James Stafford, Elisa K Liu, Jonathan Serrano, Richard Possemato, Matija Snuderl","doi":"10.1186/s40478-025-01961-w","DOIUrl":"10.1186/s40478-025-01961-w","url":null,"abstract":"<p><p>Gliomas are the most common primary brain tumors and a major source of mortality and morbidity in adults and children. Recent genomic studies have identified multiple molecular subtypes; however metabolic characterization of these tumors has thus far been limited. We performed metabolic profiling of 114 adult and pediatric primary gliomas and integrated metabolomic data with transcriptomics and DNA methylation classes. We identified that pediatric tumors have higher levels of glucose and reduced lactate compared to adult tumors regardless of underlying genetics or grade, suggesting differences in availability of glucose and/or utilization of glucose for downstream pathways. Differences in glucose utilization in pediatric gliomas may be facilitated through overexpression of SLC2A4, which encodes the insulin-stimulated glucose transporter GLUT4. Transcriptomic comparison of adult and pediatric tumors suggests that adult tumors may have limited access to glucose and experience more hypoxia, which is supported by enrichment of lactate, 2-hydroxyglutarate (2-HG), even in isocitrate dehydrogenase (IDH) wild-type tumors, and 3-hydroxybutyrate, a ketone body that is produced by oxidation of fatty acids and ketogenic amino acids during periods of glucose scarcity. Our data support adult tumors relying more on fatty acid oxidation, as they have an abundance of acyl carnitines compared to pediatric tumors and have significant enrichment of transcripts needed for oxidative phosphorylation. Our findings suggest striking differences exist in the metabolism of pediatric and adult gliomas, which can provide new insight into metabolic vulnerabilities for therapy.</p>","PeriodicalId":6914,"journal":{"name":"Acta Neuropathologica Communications","volume":"13 1","pages":"61"},"PeriodicalIF":6.2,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11909955/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143633320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cranial radiation disrupts dopaminergic signaling and connectivity in the mammalian brain.","authors":"Die Zhang, Riya Thomas, Thanh Thai Lam, Ines Veselinovic, David R Grosshans","doi":"10.1186/s40478-025-01976-3","DOIUrl":"10.1186/s40478-025-01976-3","url":null,"abstract":"<p><p>Cognitive impairment is a common and challenging side effect of cranial radiation therapy for brain tumors, though its precise mechanisms remain unclear. The mesocortical dopaminergic pathway, known to play a key role in cognitive function, is implicated in several neuropsychiatric disorders, yet its involvement in radiation-induced cognitive dysfunction is unexplored. Here, with using in vivo multi-electrode array recordings of both anesthetized and free-moving rats to monitor the firing activities of dopamine neurons in the ventral tegmental area (VTA) and local field potentials in both the prefrontal cortex (PFC) and VTA, as well as the immunofluorescence assays and western blotting, we report that cranial irradiation transiently altered VTA dopamine neuron firing patterns without affecting overall firing rates and led to sustained reductions in both \"awake\" and total dopamine neuron density. Additionally, radiation exposure impaired D2 receptor function and disrupted connectivity between the PFC and VTA. These multifaceted disruptions in the mesocortical dopamine signaling may underlie the development of radiation-induced cognitive dysfunction. These findings pave the way for novel research to prevent or reverse radiation-induced injury, ultimately improving the quality of life for brain tumor survivors.</p>","PeriodicalId":6914,"journal":{"name":"Acta Neuropathologica Communications","volume":"13 1","pages":"59"},"PeriodicalIF":6.2,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143622936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of plasma metagenomic sequencing in identification of Balamuthia mandrillaris encephalitis.","authors":"Sarah Y Edminster, Ryan W Rebbe, Christopher Khatchadourian, Kyle M Hurth, Anna J Mathew, Julie Huss-Bawab, Mark S Shiroishi, Devin Clark, Andrew P Norgan, Susan M Butler-Wu, Annie Hiniker","doi":"10.1186/s40478-025-01963-8","DOIUrl":"10.1186/s40478-025-01963-8","url":null,"abstract":"<p><p>Balamuthia mandrillaris is a rare, free-living amoeba (FLA) that causes granulomatous amoebic encephalitis, a disease with close to 90% mortality. The geographical ranges of many FLA are expanding, potentially increasing human exposure to B. mandrillaris. Here, we report a case of a 58-year-old woman with progressive neurological symptoms, ultimately diagnosed postmortem with B. mandrillaris encephalitis through plasma metagenomic next-generation sequencing (mNGS) despite negative results on both cerebrospinal fluid (CSF) mNGS and CSF PCR testing. Histologic analysis and real-time PCR (qPCR) studies on postmortem brain tissue confirmed B. mandrillaris infection with significant vascular clustering of trophozoites. Retrospective analysis of CSF mNGS data demonstrated subthreshold reads for B. mandrillaris, emphasizing the challenges of interpreting low-level pathogen signals. A systematic review of 159 published B. mandrillaris cases revealed only two reports of B. mandrillaris diagnosed using plasma mNGS, both of which also had diagnostic CSF studies. This case demonstrates the diagnostic challenges of B. mandrillaris infections, highlights its vascular tropism, and suggests that plasma mNGS may warrant evaluation as a diagnostic tool for B. mandrillaris.</p>","PeriodicalId":6914,"journal":{"name":"Acta Neuropathologica Communications","volume":"13 1","pages":"60"},"PeriodicalIF":6.2,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11908043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143622938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment of gastrointestinal function and enteric nervous system changes over time in the A53T mouse model of Parkinson's disease.","authors":"Myat Noe Han, Madeleine R Di Natale, Enie Lei, John B Furness, David I Finkelstein, Marlene M Hao, Shanti Diwakarla, Rachel M McQuade","doi":"10.1186/s40478-025-01956-7","DOIUrl":"10.1186/s40478-025-01956-7","url":null,"abstract":"<p><p>Gastrointestinal (GI) dysfunctions, including constipation and delayed stomach emptying, are prevalent and debilitating non-motor symptoms of Parkinson's disease (PD). These symptoms have been associated with damage in the enteric nervous system (ENS) and the accumulation of pathogenic alpha-synuclein (α-Syn) within the GI tract. While motor deficits and dopaminergic neuron loss in the central nervous system (CNS) of the A53T mouse model are well-characterised, the temporal relationship between GI dysfunction, ENS pathology, and motor symptoms remains unclear. This study aimed to investigate functional alterations in the GI tract at the early stages of the disease, before the appearance of motor deficits, both in vivo and ex vivo. Early colonic motility deficits observed in A53T mice, measured via bead expulsion, preceded motor impairments emerged at 36 weeks. Although whole-gut transit remained unchanged, reduced faecal output was concurrent with marked colonic dysmotility at 36 weeks. Despite a lack of significant neuronal loss, a greater number of enteric neurons in A53T mice showed signs of neuronal hypertrophy and increased nuclear translocation of HuC/D proteins indicative of neuronal stress at 12 and 36 weeks. Calcium imaging revealed differential enteric neuron activity, characterised by exaggerated calcium transients at 12 weeks that normalized by 36 weeks. Furthermore, a reduction in enteric glial populations was observed as early as 12 weeks in both the ileum and colon of A53T mice. These findings provide compelling evidence that ENS pathology, including neuronal stress, disrupted calcium signalling, and glial cell loss, precedes the onset of motor symptoms and may contribute to early GI dysfunction in PD.</p>","PeriodicalId":6914,"journal":{"name":"Acta Neuropathologica Communications","volume":"13 1","pages":"58"},"PeriodicalIF":6.2,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11899089/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143612920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Collision tumor, a metastatic melanoma within a meningioma: a case report.","authors":"Erika Yamazawa, Daniel P Cahill, Matthew P Frosch, Priscilla K Brastianos, Ryan J Sullivan","doi":"10.1186/s40478-025-01975-4","DOIUrl":"10.1186/s40478-025-01975-4","url":null,"abstract":"<p><strong>Background: </strong>Collision tumors, involving two distinct neoplasms in a single anatomical site, are rare. Among these, the metastasis of melanoma into an intracranial meningioma is particularly uncommon, with only four previously reported cases. Melanoma, known for its aggressive metastatic potential, contrasts sharply with the small number of collision tumor reports. The coexistence of these tumors poses diagnostic and therapeutic challenges, particularly in patients with a stable meningiomas.</p><p><strong>Results: </strong>We present the fifth documented case of melanoma metastasizing to a meningioma, the first to include genetic analysis revealing an NRAS mutation in the melanoma. The patient, a 58-year-old man, developed a hemorrhagic transformation of a stable left frontal meningioma. Surgical resection confirmed a biphasic tumor with melanoma cells infiltrating the meningioma. Despite initial treatment with immune checkpoint inhibitors, the patient's condition progressed with widespread metastatic melanoma, ultimately leading to death.</p><p><strong>Conclusions: </strong>The rarity of reported melanoma-to-meningioma metastasis highlights the need for further research into the genetic and pathophysiological mechanisms underlying tumor-to-tumor metastasis. Advances in genomic technologies could help identify biomarkers associated with such rare phenomena. This case also emphasizes the importance of monitoring patients with stable meningiomas and a history of melanoma for potential metastasis. Future research should explore whether prophylactic management of benign meningiomas could mitigate this risk and assess the long-term outcomes of collision tumors compared to typical metastatic brain tumors.</p>","PeriodicalId":6914,"journal":{"name":"Acta Neuropathologica Communications","volume":"13 1","pages":"57"},"PeriodicalIF":6.2,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900604/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143612921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}