Brain Pathology最新文献

{"title":"A 5-month-old infant with a pineal tumor","authors":"Fabien Forest, Martin Hasselblatt, Fanélie Barral-Clavel, Alix Clemenson, Sandrine Thouvenin, Claire Berger, Anne Mc Leer, Catherine Godfraind","doi":"10.1111/bpa.70066","DOIUrl":"10.1111/bpa.70066","url":null,"abstract":"<p>A 4-month-old child was referred to our institution due to partial epilepsy accompanied by asthenia, downward gaze deviation, and strabismus. Brain magnetic resonance imaging (MRI) showed a well delineated tumor of the pineal region in the posterior part of the third ventricle with acute hydrocephalus. The tumor was in isosignal in T1 and T2 with contrast enhancement after gadolinium injection measuring 18 mm (Figure 1). A surgical excision was decided through suboccipital transtentorial approach; during surgery, the tumor could not be completely removed because of venous invasion and because of a huge Galen vein preventing access to part of the tumor.</p><p>Histopathological analysis revealed a highly cellular tumor composed of sheets and trabecular structures made of cells with hyperchromatic nuclei and high nuclear cytoplasmic ratio, with numerous mitoses and areas of necrosis (Figure 2A and Box 1). Tubular structures containing melanin pigment were observed, as confirmed by Fontana-Masson staining (Figure 2B inset). No ganglion cell, nor rhabdomyoblastic cells, nor cells with striated muscle differentiation were found after examination, but cartilaginous-like hyalinized stroma areas were found (Figure 2C). Tumor cells stained positive for synaptophysin (Figure 1D). Expression of SMARCB1/INI1 and SMARCA4/BRG1 was retained. Stain for Lin28 was negative, while stains for Melan-A and HMB45 were weak and focal (Figure 2E,F). The Ki67/MIB1 proliferation index was 70%. Methylation testing on formalin-fixed paraffin-embedded tissue, on a tumor with tumor purity at 80% and 500 ng of DNA input with Infinium Methylation EPIC v2.0. The DNA methylation profile of the tumor did not group with any of the DKFZ classifier (version 12.8). The NIH classifier grouped the tumor with neuroblastic embryonal tumors with a score at 0.976 without a sufficient score to assess a specific tumor type. On t-SNE analysis, the DNA methylation profile grouped in the vicinity of other pineal tumors and normal pineal gland (Figure 2G).</p><p>Pineal anlage tumor, CNS WHO grade 4.</p><p>Pineal anlage tumor is regarded as a morphological variant of pineoblastoma. The histopathological hallmarks are the presence of a neuroectodermal component constituted of pineoblastoma-like cells with neuronal, glial, or melanin-containing cells combined to an ectomesenchymal component containing rhabdomyoblasts, cartilage, or smooth muscle. In the English literature, less than 30 cases have been reported [<span>1</span>]. Histopathological examination is not specific, with embryonal-like neoplastic cells growing as sheets or trabeculae, but the information of the location of the tumor is important for the diagnosis. The main differential diagnosis is atypical teratoid/rhabdoid tumors and embryonal tumor with multilayered rosettes. Pineoblastomas, so as pineal anlage tumor, retain expression of SMARCB1(INI1) and SMARCA4 (BRG1) and do not express LIN28A.</p><p>The molecular alterations of pinea","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"36 3","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13051814/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145848870","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 17-year-old male with chronic epilepsy status post remote functional hemispherectomy","authors":"Claire Voyles, Elliot Stalter, Melissa M. Blessing, Osorio Lopes Abath Neto","doi":"10.1111/bpa.70070","DOIUrl":"10.1111/bpa.70070","url":null,"abstract":"<p>A 17-year-old male with infant-onset epilepsy refractory to multiple antiseizure medications had a history of right functional hemispherectomy performed at 6 months of age after demonstration of seizure activity localized to the right frontal lobe. A brain MRI performed at 4 months of age revealed a mildly enlarged right lateral ventricle but was otherwise unremarkable. Pathology from the surgical specimen reportedly identified a focal cortical dysplasia. Follow-up visits over the years showed that the patient was nonverbal and wheelchair-dependent, with left homonymous hemianopsia and spasticity, but the epilepsy was mostly controlled with only rare brief seizures. At 17 years of age, he was found unresponsive and pronounced dead at home. Recent clinical history included a respiratory illness accompanied by vomiting, fever, and fatigue. A complete autopsy was performed, and bronchopneumonia of the left lung was established as the likely cause of death.</p><p>Gross examination of the brain revealed asymmetric cerebral hemispheres due to reduced volume of the right hemisphere, which contained a large area of cavitation spanning the frontal and temporal lobes and sparing the basal ganglia and thalamus, consistent with the history of functional hemispherectomy (Figure 1) (Box 1). Histopathological examination of sections from both hemispheres showed numerous haphazardly arranged astrocytes with eosinophilic ameboid to granular cytoplasmic inclusions (Figure 2A,B), variably distributed throughout all layers of the neocortex, and not present in deep gray matter structures. The inclusions were positive for GFAP (Figure 2C) and negative for NeuN (Figure 2D), OLIG2, PU.1, PAS, and neurofilament. There were increased numbers of corpora amylacea, highlighted by PAS.</p><p>Hyaline protoplasmic astrocytopathy.</p><p>Hyaline protoplasmic astrocytopathy (HPA) is a rare, underrecognized, and incompletely understood neuropathologic entity, with fewer than 70 cases reported in the literature, including both surgical and autopsy specimens [<span>1</span>]. First described by Alois Alzheimer in 1910 under a different designation [<span>2</span>], HPA has been associated with epilepsy, particularly in the setting of Aicardi syndrome, neurodevelopmental disorders, and less commonly, dementia.</p><p>Histopathologically, HPA is characterized by hyaline ameboid to granular astrocytic inclusions, mostly juxtanuclear, distributed throughout all cortical layers. The affected astrocytes are often enlarged and haphazardly oriented, and the inclusions are sharply demarcated and eosinophilic, distinguished from corpora amylacea or neuronal storage material by their cellular localization. Inset of Figure 2B shows a reproduction of Alzheimer's original publication showing abnormal ameboid astrocytes. The hyaline astrocytes are rarely reported in the superficial white matter, hippocampus, and basal ganglia, and are absent in other deep gray matter, cerebellum, brainstem, or sp","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"36 3","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13051899/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145970678","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":"Upregulation of sphingomyelin and ABCA8 in response to TDP-43 pathology in amyotrophic lateral sclerosis brain","authors":"Finula I. Isik,&nbsp;Russell Pickford,&nbsp;Nicolas Dzamko,&nbsp;Kerry-Anne Rye,&nbsp;Woojin Scott Kim","doi":"10.1111/bpa.70053","DOIUrl":"10.1111/bpa.70053","url":null,"abstract":"<p>Amyotrophic lateral sclerosis (ALS) is a rapidly progressing neurodegenerative disease characterized by the degeneration of motor neurons and the presence of TAR DNA-binding protein 43 (TDP-43) aggregation in the brain. Dyslipidemia is a common feature of ALS, and increasing evidence indicates that lipid dysregulation in the central nervous system underlies ALS pathology. Sphingomyelin is a sphingolipid that is highly enriched in the human brain. However, very little is known about changes in sphingomyelin in the context of ALS brain. We therefore undertook a comprehensive analysis of sphingomyelin in the disease-affected motor cortex and disease-unaffected cerebellum in sporadic ALS with TDP-43 pathology using liquid chromatography-mass spectrometry. We found that sphingomyelin was significantly increased in the ALS motor cortex compared to controls and was strongly associated with disease duration. In contrast, sphingomyelin was unaltered in the cerebellum. The increase in sphingomyelin was associated with an upregulation of ATP-binding cassette subfamily A member 8 (ABCA8), a sphingomyelin transporter, only in the motor cortex of ALS. Importantly, both sphingomyelin and ABCA8 were associated with TDP-43 only in the motor cortex. These results suggest that increases in sphingomyelin and ABCA8 could be a protective response against TDP-43 pathology.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"36 3","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13052227/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145586169","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":"Evidence of emerging transcriptome mediators of Alzheimer's disease in canine cognitive dysfunction","authors":"Shelby C. Osburn,&nbsp;Darby S. Easterday,&nbsp;Cali M. McEntee,&nbsp;Amanda S. Latham,&nbsp;Daniel S. Lark,&nbsp;Stephanie McGrath,&nbsp;Julie A. Moreno,&nbsp;Thomas J. LaRocca","doi":"10.1111/bpa.70062","DOIUrl":"10.1111/bpa.70062","url":null,"abstract":"<p>Growing data suggest companion dogs may be a promising model of human brain aging and Alzheimer's disease (AD). However, although pathology is somewhat similar in canine cognitive dysfunction (CCD) and AD, the transcriptomic similarities between these two conditions have not been thoroughly evaluated. Two emerging transcriptome-related mechanisms of human brain aging and AD involve transposable elements (TEs) and microRNAs (miRNAs), which have the potential to be carried systemically and between cells by extracellular vesicles (EVs). To determine if evidence of these AD-related transcriptomic events might be present in CCD, we generated transcriptome (RNA-seq) data on prefrontal cortex tissue and plasma EVs from young, older, and older CCD dogs. We show that: (1) global transcriptome changes with CCD indicate reduced neuronal health; (2) TE transcripts increase with CCD in both the brain and plasma EVs; (3) brain- and disease-relevant miRNAs are present in the same EVs, and some of these miRNAs correlate with indices of cognitive function/CCD. Collectively, our data suggest that transcriptomic changes in CCD, including those related to novel RNA mechanisms of brain aging and AD, may be similar to those observed in humans.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"36 3","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13051885/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145803088","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":"Evidence for different seeding activities of misfolded tau in classical and rapidly progressive Alzheimer's disease","authors":"Matthias Schmitz,&nbsp;Katrin Thüne,&nbsp;Anna-Lisa Fischer,&nbsp;Peter Hermann,&nbsp;Maria Cramm,&nbsp;Leonie Sheila Kadel,&nbsp;Wiebke Möbius,&nbsp;Jakob Matschke,&nbsp;Tayyaba Saleem,&nbsp;Neelam Younas,&nbsp;Saima Zafar,&nbsp;Hermann Altmeppen,&nbsp;Markus Glatzel,&nbsp;Inga Zerr","doi":"10.1111/bpa.70054","DOIUrl":"10.1111/bpa.70054","url":null,"abstract":"<p>Alzheimer's disease (AD) may display various clinical phenotypes with different disease progressions, such as rapidly progressive Alzheimer's disease (rpAD) type. The reason for clinical heterogeneity is still unknown and not predictable. Here, we subjected frontal cortex-derived tau seeds from classical AD, rpAD patients and controls to tau real-time quaking-induced conversion (RT-QuIC) assay analysis and examined biochemical properties, toxicity, and the morphology of tau fibrils generated during the RT-QuIC applying a cell-based assay and transmission electron microscopy (TEM). We observed seeding activity of misfolded tau protein in AD patients, which was significantly higher than in control cases. Additionally, the RT-QuIC signal response revealed differences between AD cases with a classical clinical phenotype and those with a rapidly progressive course of the disease (rpAD). The RT-QuIC reaction seeded with brain from rpAD exhibited a shorter lag phase, higher area under the curve and a higher seeding end point dilution compared to classical AD, independent from the Braak stage. The cellular toxicity of thioflavin T-positive RT-QuIC products from rpAD-seeded reactions was higher compared to those seeded by classical AD and controls. Morphological characterization of brain tissue-seeded RT-QuIC end-products via TEM showed that tau fibrils derived from rpAD seeded reactions revealed subtly different morphologies compared to classical AD. The study provides evidence for the existence of different tau assemblies in AD with different progression rates. As an alternative explanation, differences in the amounts of misfolded seed or the presence of other co-factors might influence the seeding activity of tau in AD and rpAD patients.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"36 3","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13052265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145707423","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":"Microglial reactivity and nodule formation are associated with Synaptodendritic damage in the brains of people with HIV-1","authors":"Roberta S. Dos Reis,&nbsp;Lauren A. Ignatz,&nbsp;Sathish Selvam,&nbsp;Marc C. E. Wagner,&nbsp;Sara Gianella,&nbsp;Antoine Chaillon,&nbsp;Vanessa Gomez-Moreno,&nbsp;Jeremy Martison,&nbsp;Leah H. Rubin,&nbsp;Sabina Heberlen,&nbsp;Valentina Stosor,&nbsp;Jordan Lake,&nbsp;Velpandi Ayyavoo","doi":"10.1111/bpa.70064","DOIUrl":"10.1111/bpa.70064","url":null,"abstract":"<p>Despite the success of combination antiretroviral therapy (ART) in suppressing systemic HIV replication, neurocognitive impairment (NCI) remains common among people with HIV (PWH). In the pre-ART era, severe forms such as HIV-associated dementia (HAD) were prevalent and characterized by distinct neuropathological features, including multinucleated giant cells, microglial nodules, and extensive neuronal loss. In the ART era, milder forms of NCI are more frequent; however, the underlying histopathology remains poorly understood. These milder impairments are primarily associated with synaptodendritic damage and neuronal dysregulation, typically in the absence of productive infection in neurons. Instead, microglia and macrophages are implicated as key drivers of neuroinflammation and neuronal injury. In this study, we investigated the neuropathological features of brain tissue from PWH with and without symptomatic cognitive impairment. Immunohistochemical analysis revealed microglial nodules with active neuronal phagocytosis, which was associated with dendritic loss and neuronal damage. Complementary in vitro studies demonstrated that HIV-infected microglia demonstrated enhanced phagocytic activity, supporting their direct role in neurodegeneration beyond cytokine-mediated mechanisms. Together, these findings highlight microglial phagocytosis as one of the critical contributors of HIV-associated NCI in the ART era.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"36 3","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13051873/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145854529","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":"Tau-targeting active immunotherapy slows progression and reduces pathology in mouse models of tauopathy","authors":"Christopher M. Brown,&nbsp;Jeanne K. Brooks,&nbsp;Louise Kelly,&nbsp;Madeline M. Vroom,&nbsp;Matthew Longo,&nbsp;Jean-Cosme Dodart,&nbsp;Roxana Carare,&nbsp;Justin D. Boyd","doi":"10.1111/bpa.70056","DOIUrl":"10.1111/bpa.70056","url":null,"abstract":"<p>A novel class of active immunotherapy, consisting of proprietary T-helper peptide linked to a B-cell epitope, is being developed to target tau in Alzheimer's disease (AD). These experimental therapies generate antibodies that have demonstrated binding to pathological tau in vitro, and efficacy in cell-based tau aggregation assays comparable to monoclonal antibodies. Here, we report the ability of one such tau-targeting immunotherapy, p5555kb, to prevent the progression of tau pathology using two distinct mouse models. P301L mice were immunized with p5555kb and showed greater survival rates at 210 days than saline-inoculated control mice. The efficacy of p5555kb against tau seeding in vivo was assessed by injecting C57BL6 mice with tau fibrils purified from post-mortem human AD brain tissue. Immunization with p5555kb significantly reduced the amount of tau inclusions detected by immunohistochemistry at 9 months post-injection, as compared to saline inoculation. This study demonstrates that p5555kb is effective at inducing functional tau-targeting antibodies, which prevented the onset of adverse phenotypes associated with tau pathology in vitro and in vivo.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"36 3","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13052311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145676564","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":"Frontotemporal dementia: Clinical aspects, genetics, and neuropathology of a family with a C9ORF72 expansion in Argentina","authors":"Karen Daniela Román,&nbsp;Carolina Agata Ardohain,&nbsp;Ezequiel I. Surace,&nbsp;Mónica Beatriz Mezmezian,&nbsp;Alejandro Levy,&nbsp;Alice Baez Lovera,&nbsp;Carlos Turizo,&nbsp;Marcos G. Sorbara,&nbsp;María M. Esnaola y Rojas,&nbsp;Gastón H. Graviotto,&nbsp;Gustavo Sevlever,&nbsp;Ricardo F. Allegri,&nbsp;Cecilia M. Serrano,&nbsp;Nahuel Magrath Guimet","doi":"10.1111/bpa.70057","DOIUrl":"10.1111/bpa.70057","url":null,"abstract":"<p>Frontotemporal dementia (FTD) is the second most common cause of early-onset dementia, typically manifesting before the age of 65, with a mean onset at 58 years. FTD may encompass a spectrum of neurodegenerative disorders resulting from frontotemporal lobar degeneration (FTLD), affecting behavior, language, and motor function. Among its clinical variants, the behavioral variant (bvFTD) is the most frequently inherited, often associated with mutations in MAPT, GRN, and C9ORF72, the latter being the most prevalent genetic cause of FTD and FTD-motor neuron disease (FTD-MND). While bvFTD is classically defined by profound behavioral changes and executive dysfunction, cases linked to C9ORF72 expansions exhibit atypical neuropsychiatric features. This study documents two cases within the same family presenting with bvFTD and atypical parkinsonism, associated with a C9ORF72 expansion. Neurocognitive assessments, genetic testing, and neuroimaging (MRI, SPECT) were performed to characterize the clinical phenotype. A detailed review of the familial aggregation of neurodegenerative and psychiatric disorders provided further insight into the genetic contributions to symptomatology. The findings highlight the phenotypic heterogeneity associated with C9ORF72 expansions, demonstrating a spectrum ranging from bvFTD to atypical parkinsonism, with variable neuropsychiatric involvement. While movement disorders in FTD have historically been underestimated, these cases reinforce the association between parkinsonism and familial bvFTD. Given the limited epidemiological data on genetic FTD in Latin America, this study underscores the importance of genetic testing in cases with prominent behavioral and psychiatric symptoms, supporting early identification and genetic counseling for affected families.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"36 3","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13051987/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145917092","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.70094","DOIUrl":"https://doi.org/10.1111/bpa.70094","url":null,"abstract":"&lt;p&gt;&lt;b&gt;Future International Congresses of Neuropathology (ICNs)ICN27 Edinburgh&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;ICN31 Bangalore / Bengaluru&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;Free resource: digital microscopy platform for neurodegenerative diseases curated in Munich&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 contribute suitable cases","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"36 3","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.70094","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147714969","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":"Polymorphic myopathological findings in a 77-year-old woman with oculo-bulbo-facial and distal weakness.","authors":"Michele Tosi, Angela Puma, Elena Faedo, Gianmarco Severa, Luisa Villa, Sabrina Sacconi, Edoardo Malfatti","doi":"10.1111/bpa.70099","DOIUrl":"https://doi.org/10.1111/bpa.70099","url":null,"abstract":"","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":" ","pages":"e70099"},"PeriodicalIF":6.2,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147590205","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}