Brain Pathology最新文献

{"title":"The molecular history of IDH-mutant astrocytomas without adjuvant treatment.","authors":"Zhi-Feng Shi, Kay Ka-Wai Li, Johnny Sheung-Him Kwan, Nellie Yuk-Fei Chung, Sze-Ching Wong, Abby Wai-Yan Chu, Hong Chen, Danny Tat-Ming Chan, Ying Mao, Ho-Keung Ng","doi":"10.1111/bpa.13300","DOIUrl":"https://doi.org/10.1111/bpa.13300","url":null,"abstract":"<p><p>Hypermutation and malignant transformation are potential complications arising from temozolomide treatment of IDH-mutant gliomas. However, the natural history of IDH-mutant low-grade gliomas without temozolomide treatment is actually under-studied. We retrieved retrospectively from our hospitals paired tumors from 19 patients with IDH-mutant, 1p19q non-codeleted Grade 2 astrocytomas where no interim adjuvant treatment with either temozolomide or radiotherapy was given between primary resections and first recurrences. Tissues from multiple recurrences were available from two patients and radiotherapy but not temozolomide was given before the last specimens were resected. We studied the natural molecular history of these low-grade IDH-mutant astrocytomas without pressure of temozolomide with DNA methylation profiling and copy number variation (CNV) analyses, targeted DNA sequencing, TERTp sequencing, FISH for ALT and selected biomarkers. Recurrences were mostly higher grades (15/19 patients) and characterized by new CNVs not present in the primary tumors (17/19 cases). Few novel mutations were identified in recurrences. Tumors from 17/19 (89.5%) patients showed either CDKN2A homozygous deletion, MYC or PDGFRA focal and non-focal gains at recurrences. There was no case of hypermutation. Phylogenetic trees constructed for tumors for the two patients with multiple recurrences suggested a lack of subclone development in their evolution when under no pressure from temozolomide. In summary, our studies demonstrated, in contrast to the phenomenon of temozolomide-induced hypermutation, IDH-mutant, 1p19q non-codeleted Grade 2 astrocytomas which had not been treated by temozolomide, acquired new CNVs at tumor recurrences. These findings improve our understanding of the molecular life history of IDH-mutant astrocytomas.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":" ","pages":"e13300"},"PeriodicalIF":5.8,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142543850","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":"Subcortical plaques and inflammation reflect cortical and meningeal pathologies in progressive multiple sclerosis.","authors":"Betül Okutan, Jette L Frederiksen, Gunnar Houen, Finn Sellebjerg, Cecilie Kyllesbech, Melinda Magyari, Manuela Paunovic, Per S Sørensen, Christina Jacobsen, Hans Lassmann, Stephan Bramow","doi":"10.1111/bpa.13314","DOIUrl":"https://doi.org/10.1111/bpa.13314","url":null,"abstract":"<p><p>It remains elusive whether lesions and inflammation in the sub/juxtacortical white matter reflect cortical and/or meningeal pathologies. Elucidating this could have implications for MRI monitoring as sub/juxtacortical lesions are detectable by routine MRI, while cortical lesions and meningeal inflammation are not. By large-area microscopy, we quantified total and mixed active plaque loads along with densities and sizes of perivascular mononuclear infiltrates (infiltrates) in the sub/juxtacortical white matter ≤2 mm from the cortex, intra-cortically and in the meninges. Data were related to ante-mortem clinical parameters in a false discovery rate-corrected analysis. We compared 12 patients with primary progressive multiple sclerosis (PPMS) and 15 with secondary progressive MS to 22 controls. Fifteen patients and 11 controls contributed with hemispheric sections. Sections were stained with haematoxylin-eosin, for myelin and for microglia/macrophages. B cells and T cells were confirmed in a subset. Immunoglobulin G depositions in selected cortical plaques resembled depositions described before in \"slowly expanding\" plaques in the white matter. We quantified plaque activity by measuring microglia-dominated and macrophage-dominated areas. Sub/juxtacortical plaques (load and activity) reflected plaque activity in the cerebral cortex. Plaque activity and infiltrates were more pronounced in the sub/juxtacortical white matter than in the cerebral cortex while conversely, the total plaque load was highest in the cortex. Infiltrates correlated trans-cortically and sub/juxtacortical plaque activity reflected cortical and meningeal infiltrates. Sub/juxtacortical infiltrate sizes correlated with shorter survival after progression onset. Two patients with PPMS and putatively fatal brain stem lesions argue against incidental findings. Trans-cortical inflammatory flares and plaque activity may be pathogenic in progressive MS. We suggest emphasis on sub/juxtacortical MRI lesions as plausible surrogates for cortical and meningeal pathologies and, when present, as indicators for cognitive testing.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":" ","pages":"e13314"},"PeriodicalIF":5.8,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495536","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":"Aerobic exercise improves astrocyte mitochondrial quality and transfer to neurons in a mouse model of Alzheimer's disease.","authors":"Jiachen Cai, Yan Chen, Yuzhu She, Xiaoxin He, Hu Feng, Huaiqing Sun, Mengmei Yin, Junying Gao, Chengyu Sheng, Qian Li, Ming Xiao","doi":"10.1111/bpa.13316","DOIUrl":"https://doi.org/10.1111/bpa.13316","url":null,"abstract":"<p><p>Mitochondrial dysfunction is a well-established hallmark of Alzheimer's disease (AD). Despite recent documentation of transcellular mitochondrial transfer, its role in the pathogenesis of AD remains unclear. In this study, we report an impairment of mitochondrial quality within the astrocytes and neurons of adult 5 × FAD mice. Following treatment with mitochondria isolated from aged astrocytes induced by exposure to amyloid protein or extended cultivation, cultured neurons exhibited an excessive generation of reactive oxygen species and underwent neurite atrophy. Notably, aerobic exercise enhanced mitochondrial quality by upregulating CD38 within hippocampal astrocytes of 5 × FAD mice. Conversely, the knockdown of CD38 diminished astrocytic-neuronal mitochondrial transfer, thereby abolishing the ameliorative effects of aerobic exercise on neuronal oxidative stress, β-amyloid plaque deposition, and cognitive dysfunction in 5 × FAD mice. These findings unveil an unexpected mechanism through which aerobic exercise facilitates the transference of healthy mitochondria from astrocytes to neurons, thus countering the AD-like progression.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":" ","pages":"e13316"},"PeriodicalIF":5.8,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495533","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":"CIC/ATXN1-rearranged tumors in the central nervous system are mainly represented by sarcomas: A comprehensive clinicopathological and epigenetic series.","authors":"Arnault Tauziède-Espariat, Azadeh Ebrahimi, Nathalie Boddaert, Torsten Pietsch, Wieslawa Grajkowska, Tobias Blau, Arend Koch, Philipp Sievers, Delphine Guillemot, Gaëlle Pierron, Emmanuelle Uro-Coste, Yvan Nicaise, Aurore Siegfried, Adam Gilles, Franck Bielle, Karima Mokhtari, Dominique Cazals-Hatem, Gueorgui Iakovlev, Benoît Lhermitte, Natacha Entz-Werle, Marie Csanyi, Claude-Alain Maurage, Victor Legrand, Jean Boutonnat, Catherine Godfraind, Anne McLeer, Lauren Hasty, Alice Métais, Oumaima Aboubakr, Thomas Blauwblomme, Kévin Beccaria, Volodia Dangouloff-Ros, Pascale Varlet","doi":"10.1111/bpa.13303","DOIUrl":"https://doi.org/10.1111/bpa.13303","url":null,"abstract":"<p><p>CIC fusions have been described in two different central nervous system (CNS) tumor entities. On one hand, fusions of CIC or ATXN1 genes belonging to the same complex of transcriptional repressors, were reported in the CIC-rearranged, sarcoma (SARC-CIC). The diagnosis of this tumor type, which was recently added to the World Health Organization (WHO) Classification of CNS tumors, is difficult mainly because the data concerning its histopathology (as compared to its soft tissue counterpart), immunoprofile, and clinical as well as radiological characteristics are scarce in the literature. On the other hand, a recent study, based on DNA-methylation profiling, has identified a novel high-grade neuroepithelial tumor characterized by recurrent CIC fusions (HGNET-CIC). The aim of this multicentric study was to characterize a cohort of 15 primary CNS tumors harboring a CIC or ATXN1 fusion in terms of clinical, radiological, histopathological, immunophenotypical, and epigenetic characteristics. According to the integrated diagnoses, 14/15 tumors corresponded to SARC-CIC, and only one to HGNET-CIC. The tumors showed similar clinical (mainly pediatric), radiological (mostly supratentorial, cystic, and contrast enhancing), immunophenotypical (common expression of glioneuronal markers), and genetic (similar spectrum of fusions) profiles but their histopathological appearance was clearly distinct. Moreover, we found a novel fusion transcript (CIC::EWSR1) in a SARC-CIC. Most DNA methylation profiles using the Heidelberg Brain Tumor Classifier (v12.8) annotated the samples to the methylation class \"SARC-CIC\" (9/14 tumors with available data). By using uniform manifold approximation and projection analysis, four other samples were classified as SARC-CIC and another clustered within the methylation class of HGNET-CIC. Our findings confirm that CNS CIC-fused tumors do not represent a single molecular tumor entity. Further analyses are needed to characterize HGNET-CIC in more detail. These results may help to refine the essential diagnostic criteria for SARC-CIC and their terminology (with a suggested consensual name of sarcoma, CIC/ATXN1-complex rearranged).</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":" ","pages":"e13303"},"PeriodicalIF":5.8,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495534","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":"Nicorandil treatment improves survival and spatial learning in aged granulin knockout mice.","authors":"Dana M Niedowicz, Wang-Xia Wang, Paresh Prajapati, Yu Zhong, Shuling Fister, Colin B Rogers, Pradoldej Sompol, David K Powell, Indumati Patel, Christopher M Norris, Kathryn E Saatman, Peter T Nelson","doi":"10.1111/bpa.13312","DOIUrl":"https://doi.org/10.1111/bpa.13312","url":null,"abstract":"<p><p>Mutations in the human granulin (GRN) gene are associated with multiple diseases, including dementia disorders such as frontotemporal dementia (FTD) and limbic-predominant age-related TDP-43 encephalopathy (LATE). We studied a Grn knockout (Grn-KO) mouse model in order to evaluate a potential therapeutic strategy for these diseases using nicorandil, a commercially available agonist for the ABCC9/Abcc9-encoded regulatory subunit of the \"K⁺ATP\" channel that is well-tolerated in humans. Aged (13 months) Grn-KO and wild-type (WT) mice were treated as controls or with nicorandil (15 mg/kg/day) in drinking water for 7 months, then tested for neurobehavioral performance, neuropathology, and gene expression. Mortality was significantly higher for aged Grn-KO mice (particularly females), but there was a conspicuous improvement in survival for both sexes treated with nicorandil. Grn-KO mice performed worse on some cognitive tests than WT mice, but Morris Water Maze performance was improved with nicorandil treatment. Neuropathologically, Grn-KO mice had significantly increased levels of glial fibrillary acidic protein (GFAP)-immunoreactive astrocytosis but not ionized calcium binding adaptor molecule 1 (IBA-1)-immunoreactive microgliosis, indicating cell-specific inflammation in the brain. Expression of several astrocyte-enriched genes, including Gfap, were also elevated in the Grn-KO brain. Nicorandil treatment was associated with a subtle shift in a subset of detected brain transcript levels, mostly related to attenuated inflammatory markers. Nicorandil treatment improved survival outcomes, cognition, and inflammation in aged Grn-KO mice.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":" ","pages":"e13312"},"PeriodicalIF":5.8,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495535","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":"Society News","authors":"","doi":"10.1111/bpa.13308","DOIUrl":"https://doi.org/10.1111/bpa.13308","url":null,"abstract":"","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"34 6","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.13308","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142447543","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":"40-Year-old man with two asynchronous spinal cord tumors","authors":"Maximilian Bschorer,&nbsp;Matthias Dottermusch,&nbsp;Jakob Matschke,&nbsp;Jens Gempt,&nbsp;Ulrich Schüller,&nbsp;Malte Mohme","doi":"10.1111/bpa.13309","DOIUrl":"10.1111/bpa.13309","url":null,"abstract":"&lt;p&gt;A 38-year-old individual presented with intermittent bladder dysfunction, radicular pain, and mild foot elevator paresis. After an emergency lumbar MRI revealed a vertebral disc herniation at the L5/S1 level, an emergency sequestrectomy was performed. Although the radicular pain resolved postoperatively, the patient's bladder voiding dysfunction worsened. Further MRI imaging revealed a contrast-enhancing intramedullary lesion at the TH11/TH12 spinal levels (Figure 1A).&lt;/p&gt;&lt;p&gt;The patient was transferred to the neurosurgical department for further treatment, and urgent surgery was performed with continuous intraoperative neurophysiological monitoring. Histopathological analysis was conducted and subsequent DNA methylation analysis confirmed the histological diagnosis. The patient did not undergo genetic testing for neurofibromatosis (NF), as he did not exhibit any other typical features or tumors associated with NF.&lt;/p&gt;&lt;p&gt;Postoperative paraparesis and bladder dysfunction were promptly resolved in neurological rehabilitation, resulting in a McCormick score of one. Three years later, the patient presented with new radiculopathy in both legs accompanied and hypesthesia. MRI showed a new contrast-enhancing lesion at L2/L3, which was located at a distance from the previous lesion (Figure 1B). The patient underwent surgery for this symptomatic lesion. The histopathological and methylation analysis revealed a distinct diagnosis, when compared to the histological examination of the initial tumor. Postoperative imaging showed no residual tumor, and there were no other central nervous system (CNS) manifestations of the tumor. The patient's rapid recovery from neurological symptoms allowed for discharge to ambulatory service.&lt;/p&gt;&lt;p&gt;Histological comparison of the first and second tumor revealed distinctive features. The first tumor was characterized by isomorphic glial cells with round nuclei within a delicate fibrillary matrix, as observed in H&amp;E staining (Figure 2, Box 1). The tumor cells showed clear expression of glial fibrillary acidic protein (GFAP), but not OLIG2 or NMYC. The Ki67 labeling index was below 5% of the tumor cell nuclei. Zones without nuclei around blood vessels, known as perivascular pseudorosettes, were also present.&lt;/p&gt;&lt;p&gt;The second tumor was characterized by more spindled tumor cells within a coarse myxoid glial matrix, indicative of a divergent histological diagnosis. The cell nuclei were oval to elongated with slightly loosened nuclear chromatin. Similar to the first tumor, strong GFAP immunostaining was observed. The second tumor was distinctively marked by nuclear expression of HOXB1, absent in the first tumor.&lt;/p&gt;&lt;p&gt;For both samples, DNA methylation data were obtained using the Illumina Human MethylationEPIC (850 k) array bead chips. The classification of brain tumors based on DNA methylation was performed using the publicly available “classifier” tool, version v12.8 (www.molecularneuropathology.org/mnp). The epigenetic anal","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"34 6","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.13309","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380079","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 55-year-old man with a cerebral mass","authors":"Serena Ammendola,&nbsp;Giuseppe Kenneth Ricciardi,&nbsp;Valeria Barresi","doi":"10.1111/bpa.13310","DOIUrl":"10.1111/bpa.13310","url":null,"abstract":"&lt;p&gt;A 55-year-old man presented with recent onset of dizziness and left lower limb weakness. Magnetic resonance imaging revealed a relatively circumscribed mass in the left frontal lobe extending to the corpus callosum and contralateral hemisphere, with conspicuous perilesional edema and contrast enhancement (Figure 1). A whole-body computerized tomography (CT) scan did not reveal any other lesions. The patient underwent partial excision of the mass. F-18 fluorodeoxyglucose–positron emission tomography (PET) imaging demonstrated hypermetabolism in the residual brain mass, but no evidence of any lesion outside the central nervous system.&lt;/p&gt;&lt;p&gt;Microscopic examination revealed a hypercellular neoplasm mainly composed of large cells exhibiting irregular or indented, frequently nucleolated, nuclei, and eosinophilic cytoplasm, and characterized by brisk mitotic activity (Figure 2A; Box 1) and necrosis. Additionally, scattered binucleated or multinucleated cells were observed (Figure 2A). Some neoplastic cells exhibited hemophagocytic activity, consisting of engulfment of fragmented neutrophils or red blood cells in the cytoplasm (Figure 2B), whereas others displayed a brown cytoplasmic pigment (Figure 2C). Perl's staining revealed the presence of iron deposits in these cells (Figure 2D). Immunohistochemistry showed that the tumor cells were diffusely positive for CD68 (Figure 2E), CD163 (Figure 2F), and CD45, and negative for CD3, CD20, CD30, ALK, Langerin (CD207), CD21, myeloperoxidase, CD34, CD117, HMB45, Melan-A, CKAE1-AE3, GFAP, and OLIG2. CD4 (Figure 2G) and S100 positivity was observed in some neoplastic cells (Figure 2). Ki-67 labeling index was 40%. Immuno-expression of BRAF p. V600E was absent. CD3 immunostaining revealed abundant infiltration of small lymphocytes (Figure 2H).&lt;/p&gt;&lt;p&gt;Histiocytic sarcoma (HS).&lt;/p&gt;&lt;p&gt;HS is an exceedingly rare and aggressive hematopoietic tumor that primarily affects the lymph nodes, skin, gastrointestinal tract, or soft tissues, and can occur in individuals of varying ages, ranging from infancy to older adulthood. Primary HS of the central nervous system (CNS) is extremely uncommon, with fewer than 40 cases reported in the English literature [&lt;span&gt;1&lt;/span&gt;]. Herein we present an additional case, which was considered as primary HS of the CNS owing to the lack of localization outside the CNS on CT and PET scans. According to the World Health Organization classification of CNS tumors, HS is defined as a malignant proliferation of cells showing morphological and immunophenotypic features of histiocytes and no other lines of differentiation. Histologically, HS is characterized by large cells with irregular nucleolated nuclei and eosinophilic cytoplasm, and brisk mitotic activity. An infiltrate of lymphocytes surrounding tumor cells, along with the presence of large pleomorphic cells and CD45 positivity may suggest anaplastic large-cell lymphoma or diffuse large B-cell lymphoma. However, the absence of immunostaining ","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"34 6","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.13310","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142370972","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":"hnRNP A1, hnRNP A2B1, and hnRNP K are dysregulated in tauopathies, but do not colocalize with tau pathology.","authors":"Tomas Kavanagh, Kaleah Balcomb, Diba Ahmadi Rastegar, Guinevere F Lourenco, Thomas Wisniewski, Glenda Halliday, Eleanor Drummond","doi":"10.1111/bpa.13305","DOIUrl":"https://doi.org/10.1111/bpa.13305","url":null,"abstract":"<p><p>Tau interacts with multiple heterogeneous nuclear ribonucleoproteins (hnRNPs)-a family of RNA binding proteins that regulate multiple known cellular functions, including mRNA splicing, mRNA transport, and translation regulation. We have previously demonstrated particularly significant interactions between phosphorylated tau and three hnRNPs (hnRNP A1, hnRNP A2B1, and hnRNP K). Although multiple hnRNPs have been previously implicated in tauopathies, knowledge of whether these hnRNPs colocalize with tau aggregates or show cellular mislocalization in disease is limited. Here, we performed a neuropathological study examining the colocalization between hnRNP A1, hnRNP A2B1, hnRNP K, and phosphorylated tau in two brain regions (hippocampus and frontal cortex) in six disease groups (Alzheimer's disease, mild cognitive impairment, progressive supranuclear palsy, corticobasal degeneration, Pick's disease, and controls). Contrary to expectations, hnRNP A1, hnRNP A2B1, and hnRNP K did not colocalize with AT8-immunoreactive phosphorylated tau pathology in any of the tauopathies examined. However, we did observe significant cellular mislocalization of hnRNP A1, hnRNP A2B1 and hnRNP K in tauopathies, with unique patterns of mislocalization observed for each hnRNP. These data point to broad dysregulation of hnRNP A1, A2B1 and K across tauopathies with implications for disease processes and RNA regulation.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":" ","pages":"e13305"},"PeriodicalIF":5.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361119","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":"Posterior pituitary tumors and other rare entities involving the pituitary gland.","authors":"Federico Roncaroli, Caterina Giannini","doi":"10.1111/bpa.13307","DOIUrl":"https://doi.org/10.1111/bpa.13307","url":null,"abstract":"<p><p>Non-neuroendocrine tumors account for around 10% of all primary neoplasms of the sella. If meningiomas, craniopharyngiomas, and germ cell tumors are excluded, the remaining lesions include a broad spectrum of uncommon, benign, and aggressive, often diagnostically challenging lesions. This review aims to summarize the essential clinicopathological features of tumors of the posterior pituitary gland, infundibulum spectrum expressing thyroid transcription factor 1, and primary sellar atypical rhabdoid teratoid tumor, and provide the criteria for their diagnosis and management.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":" ","pages":"e13307"},"PeriodicalIF":5.8,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342010","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}