Brain Pathology最新文献

{"title":"Lewy bodies are surrounded by granulovacuolar degeneration bodies in dementia with Lewy bodies.","authors":"Searlait Thom, Pawel Palmowski, Andrew Porter, Joe O'Neill, Johannes Attems, Laura A Smith, Viktor I Korolchuk, Daniel Erskine","doi":"10.1111/bpa.70119","DOIUrl":"https://doi.org/10.1111/bpa.70119","url":null,"abstract":"<p><p>Lewy bodies (LBs), composed primarily of aggregated α-synuclein (α-syn), are the pathological hallmark of Lewy body diseases, including Parkinson's disease, Parkinson's disease dementia and dementia with Lewy bodies (DLB). Despite their diagnostic significance, the mechanisms underlying LB formation and their contribution to neurodegeneration remain poorly understood. Previous studies have reported that structures labelled with ubiquitin phosphorylated at serine 65 (p-Ub^S65)-a marker of mitophagy-localise both at the periphery of and within LBs. This study aimed to further characterise these structures and clarify their relationship to α-syn pathology in DLB. Immunofluorescence analysis of post-mortem DLB brain tissue revealed intermittent co-localisation of p-Ub^S65+ puncta with conventional mitochondrial markers. Given previous findings that granulovacuolar degeneration bodies (GVBs)-vesicular structures frequently associated with tau pathology, itself a concomitant feature of DLB-are immunopositive for p-Ub^S65, we next examined whether peri-LB p-Ub^S65+ structures are actually GVBs. p-Ub^S65 puncta co-stained with established GVB markers including charged multivesicular body protein 2B (CHMP2B) and casein kinase 1 delta (CK1D), and, more variably with hyperphosphorylated tau (AT8), across multiple brain regions associated with LB pathology. Notably, GVB abundance within the anterior cingulate gyrus was found to positively correlate with p-α-syn^S129 burden. In summary, p-Ub^S65+ GVBs, containing both auto- and endolysosomal material, cluster around LBs in DLB. Frequently immunoreactive for tau, these hybrid waste vesicles provide a tangible mechanistic link between α-syn and tau pathology and may offer new insight into the processes underlying LB formation in DLB.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":" ","pages":"e70119"},"PeriodicalIF":5.0,"publicationDate":"2026-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148306957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A 3-year-old girl with a left optic nerve tumor.","authors":"Samuel López Muñoz, Alberto Berjón, Carlos Rodríguez Antolín, Claudia Sánchez Lara, Marta Mendiola, Victoria Heredia Soto, Álvaro Lassaletta, Carlos González Pérez, Pedro Rubio Aparicio, Jorge Zamorano, Isabel Esteban Rodríguez","doi":"10.1111/bpa.70116","DOIUrl":"https://doi.org/10.1111/bpa.70116","url":null,"abstract":"","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":" ","pages":"e70116"},"PeriodicalIF":5.0,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148300994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chromosomal and immune dysregulation underlying granular mitosis in glioblastoma.","authors":"Rachel Barboza, Xuan Wang, August Lin, Eric Liu, Pramath Kakodkar, Yayuan Zhao, Quinn Le, Christina A Castellani, Qi Zhang","doi":"10.1111/bpa.70115","DOIUrl":"https://doi.org/10.1111/bpa.70115","url":null,"abstract":"<p><p>Granular mitosis (GM) is a distinctive form of atypical mitosis characterized by dispersed chromosomal granules within the mitotic figure. Although described morphologically in glioblastoma, its molecular etiology has remained unknown. Data from The Cancer Genome Atlas (TCGA) Glioblastoma Multiforme cohort was analyzed. AI-assisted digital pathology was used to annotate mitotic figures, including GM, on hematoxylin and eosin-stained whole-slide images. Corresponding transcriptomic and genomic data were subjected to differential gene expression and copy number variation (CNV) analyses, followed by overrepresentation testing to identify enriched biological pathways. Clinical data were correlated to assess associations with molecular and pathological findings. Validation was performed on an independent glioblastoma cohort using immunohistochemistry. Sixty-three glioblastoma cases were included (32 GM-positive, 31 GM-negative). Transcriptomic analysis identified 185 differentially expressed genes (FDR <0.05; log₂FC >1.5). GM-positive tumors demonstrated broad downregulation of genes involved in nucleosome assembly, protein-DNA complex organization, and centromeric differentiation, alongside significant suppression of PI3K-Akt signaling (p = 5.58 × 10^-5). Unexpectedly, immune-related pathways-including Neutrophil extracellular trap (NET) formation and Cytokine-cytokine receptor interaction-were similarly underexpressed, indicating global suppression of innate immune signaling in GM-positive glioblastomas. Two CNVs were associated with a higher proportion of GM, demonstrating chromosomal fragility. Immunohistochemistry revealed a significantly higher density of immune cells, particularly macrophages and antigen-presenting cells, in close proximity to granular mitoses. Spatial correlation analysis demonstrated positive correlations between GM distribution and immune cell density across tumor regions. This study provides the first comprehensive molecular characterization of granular mitosis in glioblastoma. The findings link GM morphology to chromosomal disorganization, PI3K/PTEN pathway alterations, and impaired innate immunity, suggesting that GM represents a histologic correlate of centromeric stress and immune impairment in glioblastomas. Notably, granular mitoses are associated with localized immune cell enrichment and exhibit a positive spatial correlation with immune cell density within their microenvironment.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":" ","pages":"e70115"},"PeriodicalIF":5.0,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148283348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nearest-neighbors assisted unsupervised analysis for methylation array profiling for central nervous system tumors.","authors":"Mallika Gandham, Surendra Dasari, Cherisse Marcou, Stephanie Smoley, Matthew Isaacson, Caterina Giannini, Aditya Raghunathan, Rachael A Vaubel, M Adelita Vizcaino Villalobos, Aivi Nguyen, Jorge A Trejo-Lopez, Kenneth Aldape, Cristiane M Ida","doi":"10.1111/bpa.70117","DOIUrl":"https://doi.org/10.1111/bpa.70117","url":null,"abstract":"<p><p>The NN method identifies the five nearest reference dataset neighbors to a tested sample and provides an objective estimation of the tested sample methylation class cluster rather than relying on subjective visualization using dimensionality reduction methods such as UMAP and t-SNE.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":" ","pages":"e70117"},"PeriodicalIF":5.0,"publicationDate":"2026-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148276001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A highly abundant circular RNA from the RMST locus plays a role in posterior fossa ependymoma pathogenesis","authors":"Ulvi Ahmadov,&nbsp;Charlotte W. Udengaard,&nbsp;Stine M. Vissing,&nbsp;Silke D. Nielsen,&nbsp;Kim-Gwendolyn Dietrich,&nbsp;Benedicte Parm Ulhøi,&nbsp;Lasse S. Kristensen","doi":"10.1111/bpa.70071","DOIUrl":"10.1111/bpa.70071","url":null,"abstract":"<p>Pediatric ependymoma (EPN) is one of the most common central nervous system cancers in children often accompanied by a poor prognosis. The circular RNA, circRMST, is known to be upregulated in posterior fossa (PF) EPN, but its functional role in the disease has not been explored. We found that circRMST is abundantly expressed in the cytoplasm of cancer cells in PF EPN patients. Moreover, knockdown of circRMST in EPN cancer stem cell-like cells induced differentiation-related pathways while the expression of cell cycle-related pathways was reduced, suggesting that it acts as an oncogene. We further validated these findings using flow cytometry-based cell cycle analysis and an in vitro serum-induced differentiation assay. Furthermore, we found that high circRMST expression and low promoter methylation levels are associated with poor prognosis. In conclusion, this study identifies circRMST as a novel oncogene in PF EPN.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"36 4","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.70071","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145997351","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":"Rapid generation of prion disease models using AAV-delivered PrP variants in knockout mice","authors":"Maitena San-Juan-Ansoleaga,&nbsp;Eva Fernández-Muñoz,&nbsp;Jorge M. Charco,&nbsp;Enric Vidal,&nbsp;Diego Herrero-Martínez,&nbsp;Josu Galarza-Ahumada,&nbsp;Cristina Sampedro-Torres-Quevedo,&nbsp;Samanta Giler,&nbsp;Mariví Geijo,&nbsp;Gloria González-Aseguinolaza,&nbsp;Hasier Eraña,&nbsp;Joaquín Castilla","doi":"10.1111/bpa.70077","DOIUrl":"10.1111/bpa.70077","url":null,"abstract":"<p>The study of prion biology has traditionally relied on transgenic mouse models, which, while valuable, require significant time and resources to develop. Here, we present a rapid and flexible alternative using adeno-associated virus (AAV) vectors to express modified prion proteins in PrP-knockout (PrP-KO) mice. Through systematic evaluation of multiple AAV constructs, we optimized vector design by comparing different CNS-specific promoters and regulatory elements to generate prion disease models capable of faithfully propagating the inoculated prion strain. We identified an optimized AAV construct incorporating the human synapsin promoter, MVM enhancer, and WPRE posttranscriptional regulatory element encapsidated in the AAV9P31 serotype to drive neuron-specific expression of modified mouse PrP (W144Y epitope) and bank vole I109 PrP (W145Y epitope). Following intravenous administration, we achieved brain-wide expression at levels comparable to or even exceeding endogenous PrP in some regions. When challenged with mouse-adapted RML prions or human Gerstmann-Sträussler-Scheinker (GSS-A117V) disease-causing prions, AAV-PrP mice developed characteristic signs of prion disease with accelerated kinetics (58–106 days post-inoculation for RML; 105–112 dpi for GSS-A117V), displaying features typical of each strain. Serial transmission of AAV-generated RML prions to wild-type mice confirmed preservation of strain-specific properties (165 ± 4 dpi), validating the authenticity of prion propagation in this system. This approach provides a versatile platform for rapidly generating and studying prion variants in an authentic brain environment. By reducing model generation time from months to weeks, this system enables accelerated investigation of prion structure–function relationships, strain properties, and therapeutic strategies, with potential applications extending to other protein misfolding diseases.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"36 4","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.70077","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146092045","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":"Immunohistochemistry as a tool for identifying EGFR amplification in CNS tumors","authors":"Arnault Tauziède-Espariat,&nbsp;Mary Bah,&nbsp;Farah Sassi,&nbsp;Noémie Pucelle,&nbsp;Charlotte Berthaud,&nbsp;Marion Mandoula,&nbsp;Zeina Dababou,&nbsp;Noah Carnes,&nbsp;Leïla Brissez,&nbsp;Lauren Hasty,&nbsp;Euphrasie Servant,&nbsp;Alice Métais,&nbsp;Pascale Varlet","doi":"10.1111/bpa.70073","DOIUrl":"10.1111/bpa.70073","url":null,"abstract":"<p><i>EGFR</i> gene amplification constitutes a diagnostic hallmark for glioblastoma, IDH-wildtype (GB, IDH-WT). Herein, we demonstrated that EGFR IHC is a highly specific and sensitive biomarker for identifying <i>EGFR</i> amplification and should be part of the neuropathologist's routine panel of antibodies.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"36 4","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.70073","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148148630","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":"Integrated high-resolution copy number and histomolecular analysis of diffuse hemispheric glioma, H3 G34-mutant reveals universal TP53 abnormalities","authors":"Jorge A. Trejo-Lopez,&nbsp;Cinthya Zepeda Mendoza,&nbsp;Thomas M. Kollmeyer,&nbsp;Kristen L. Drucker,&nbsp;Vanessa M. Pazdernik,&nbsp;Paul A. Decker,&nbsp;Corinne E. Praska,&nbsp;Jayson Hardcastle,&nbsp;Stephanie Smoley,&nbsp;Matthew Isaacson,&nbsp;Mallika Gandham,&nbsp;Surendra Dasari,&nbsp;Aditya Raghunathan,&nbsp;Caterina Giannini,&nbsp;Gang Zheng,&nbsp;Aaron Wagner,&nbsp;M. Beatriz Lopes,&nbsp;Kar-Ming A. Fung,&nbsp;JoElle G. Peterson,&nbsp;Andreana L. Rivera,&nbsp;Christopher Rossi,&nbsp;Meggen A. Walsh,&nbsp;Zied Abdullaev,&nbsp;Kenneth Aldape,&nbsp;Martha Quezado,&nbsp;Drew Pratt,&nbsp;Patrick Joseph Cimino,&nbsp;Robert B. Jenkins,&nbsp;Cristiane M. Ida","doi":"10.1111/bpa.70076","DOIUrl":"10.1111/bpa.70076","url":null,"abstract":"<p>Diffuse hemispheric glioma, H3 G34-mutant (DHG-H3 G34) has been primarily molecularly characterized by methylation profiling and sequencing studies. We describe an integrated histomolecular evaluation including high-resolution copy number profiling of a series of 60 DHG-H3 G34 to further our understanding of the spectrum of genetic changes associated with this tumor type. Cases were clinically tested using an 187-gene mutation and fusion targeted neuro-oncology next-generation sequencing panel (<i>n</i> = 60) and Oncoscan chromosomal microarray (<i>n</i> = 26) by a single laboratory (2018–2022). A subset of cases had immunohistochemical results for OLIG2 (<i>n</i> = 42), p53 (<i>n</i> = 48), and ATRX (<i>n</i> = 46), and methylation array data (<i>n</i> = 8). Median age at testing was 21 years (range, 12–50). No significant difference was noted in clinical, histopathological, and mutational profile between pediatric and adult patients. <i>H3-3A</i> G34 mutations included G34R (<i>n</i> = 56; 94%), G34V (<i>n</i> = 3), and a non-canonical G34E (<i>n</i> = 1). Concurrent mutations most often involved <i>TP53</i> (<i>n</i> = 55; 92%), <i>ATRX</i> (<i>n</i> = 50; 83%), and <i>PDGFRA</i> (<i>n</i> = 34; 57%). A reportedly primary tumor was confirmed to be hypermutant and had a <i>PMS2</i> mutation. A single case also showed an <i>FGFR3::FAM184B</i> fusion. All cases with available chromosomal microarray data had unbalanced genomes, which were often complex (14/26; 54%). The most frequent recurrent copy number abnormalities were losses involving 3q, 4q, 10q, 13q, and 18q, and 17p copy-neutral loss of heterozygosity (cnLOH) encompassing <i>TP53</i>. This copy number profile was reminiscent of that seen in Grade 4 IDH-mutant astrocytomas. Collectively, a <i>TP53</i> abnormality at copy number (12/26, all cnLOH), sequence (55/60) and protein expression (46/48) level was detected in all 60 cases. In conclusion, integrated high-resolution copy number and histomolecular analysis expanded the spectrum of genetic changes associated with DHG-H3 G34, including the presence of universal <i>TP53</i> abnormalities with frequent cnLOH—a copy number abnormality that has been largely unrecognized—for this new 2021 World Health Organization central nervous system tumor type.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"36 4","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.70076","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123888","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":"A muscular dystrophy associated with bi-allelic LEMD2 variants: Expanding the genotype of nuclear envelopathies","authors":"Marc Pauper,&nbsp;Heike Kölbel,&nbsp;Iakowos Karakesisoglou,&nbsp;Anne Schänzer,&nbsp;Johann Böhm,&nbsp;Rachel Thompson,&nbsp;Nicolai Kohlschmidt,&nbsp;Bernd Ringel,&nbsp;Gisèle Bonne,&nbsp;Katja Neuhoff,&nbsp;Andrea Gangfuß,&nbsp;Ozge Aksel Kilicarslan,&nbsp;Sergi Beltran Agullo,&nbsp;Andreas Hentschel,&nbsp;Ulrike Schara-Schmidt,&nbsp;Hanns Lochmüller,&nbsp;Kiran Polavarapu,&nbsp;Andreas Roos","doi":"10.1111/bpa.70082","DOIUrl":"10.1111/bpa.70082","url":null,"abstract":"<p>Proteomics-guided exome re-analysis identifies bi-allelic variants in the nuclear envelope LEMD2 gene, expanding its phenotypic spectrum. Created in BioRender. Pauper, M. (2026) https://BioRender.com/xamvo92.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"36 4","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.70082","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147347247","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":"SOCIETY NEWS","authors":"Audrey Rousseau","doi":"10.1111/bpa.70107","DOIUrl":"https://doi.org/10.1111/bpa.70107","url":null,"abstract":"&lt;p&gt;&lt;b&gt;&lt;i&gt;Future International Congresses of Neuropathology (ICNs)ICN27 Edinburgh&lt;/i&gt;&lt;/b&gt;. The International Congress of Neuropathology (ICN) will be held in Edinburgh, Scotland, in 2027 (ICN27). The Congress President will be Prof Colin Smith and the ICN27 will be hosted by the British Neuropathological Society (BNS).&lt;/p&gt;&lt;p&gt;“On behalf of the British Neuropathological Society I am delighted to extend a warm invitation to all our colleagues across the world to join us in Edinburgh for the International Congress of Neuropathology 2027. Edinburgh is an easily accessible centre, surrounded by 1000 years of living history. We will develop a strong academic programme covering all aspects of neuropathology with world leading plenary speakers, supported by a social programme highlighting some of Edinburgh's historic charms. For those wishing to explore further, Edinburgh offers access to many of Scotland's highlights, be it touring the Highlands, sampling our famous whisky or golfing on some of our picturesque courses. I do hope you will be able to join us for what I am sure will be a memorable meeting showcasing the best in international neuropathology.&lt;/p&gt;&lt;p&gt;Colin Smith&lt;/p&gt;&lt;p&gt;Congress President ISN 2027”&lt;/p&gt;&lt;p&gt;&lt;b&gt;&lt;i&gt;ICN31 Bangalore / Bengaluru&lt;/i&gt;&lt;/b&gt;. ISN is pleased to announce that the International Congress of Neuropathology 2031 (ICN31) will be hosted in Bangalore/Bengaluru, India, following a successful bid from the Neuropathology Society of India (NPSI). The congress is planned for the beginning of October 2031 (final dates to be confirmed). It will be the first time for the International Congress of Neuropathology to take place in India and we very much look forward to it. Congratulations to NPSI for preparing to host the first International Congress of Neuropathology in India. We will be receiving regular updates on congress planning and preparations including more formal updates at our Joint ISN Council &amp; Executive meetings in the coming years.&lt;/p&gt;&lt;p&gt;Summary report for ICN23 Berlin (our most recent International Congress of Neuropathology, September 2023) now available in the Society's journal Brain Pathology (see link: https://doi.org/10.1111/bpa.13249).&lt;/p&gt;&lt;p&gt;&lt;b&gt;&lt;i&gt;Brain Pathology has joined Wiley's Open Access&lt;/i&gt;&lt;/b&gt; portfolio as of January 2021. As a result, all submissions are subject to an Article Publication Charge (APC) if accepted and published in the journal. ISN members are eligible for a 10% discount off the Open Access APC. For more information on the fees, please click here.&lt;/p&gt;&lt;p&gt;&lt;b&gt;&lt;i&gt;Free resource: digital microscopy platform for neurodegenerative diseases curated in Munich&lt;/i&gt;&lt;/b&gt;. Prof Jochen Herms and his team have been setting up a digital microscopy platform for neurodegenerative diseases in their department in Munich. Registration is free. ISN members and interested colleagues are invited to use this resource, which will be particularly useful for teaching and training (see link below). Colleagues are invited to cont","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"36 4","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.70107","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148153583","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}