Each year hundreds of reviewers contribute their expertise to peer review, a process that contributes critically to the quality of the Brain Pathology. The editors at Brain Pathology would like to extend their gratitude to those who have provided their time and energy to review manuscripts for our journal over the last year. We are well aware that our journal can only exist thanks to your concerted efforts to provide concise, accurate, and thoughtful reviews. Below is a list of all of you who completed at least one review, and agreed to have your name published. We also thank those reviewers who choose not to have their names published.
{"title":"Acknowledgement to Reviewers","authors":"","doi":"10.1111/bpa.13220","DOIUrl":"https://doi.org/10.1111/bpa.13220","url":null,"abstract":"<p>Each year hundreds of reviewers contribute their expertise to peer review, a process that contributes critically to the quality of the Brain Pathology. The editors at Brain Pathology would like to extend their gratitude to those who have provided their time and energy to review manuscripts for our journal over the last year. We are well aware that our journal can only exist thanks to your concerted efforts to provide concise, accurate, and thoughtful reviews. Below is a list of all of you who completed at least one review, and agreed to have your name published. We also thank those reviewers who choose not to have their names published.</p><p>Ahrendsen, Jared</p><p>Alexandrescu, Sanda</p><p>Auer, Roland</p><p>Ayton, Scott</p><p>Battini, Jean-Luc</p><p>Bieniek, Kevin</p><p>Bockmayr, Michael</p><p>Cai, Jinquan</p><p>Carare, Roxana</p><p>Cullell, N</p><p>Del Bigio, Marc</p><p>Dudek, Ed</p><p>Englert, Benjamin</p><p>Evelson, Pablo</p><p>Falkenburger, Björn</p><p>Ferrer, Isidre</p><p>Gilani, Ahmed</p><p>Giustetto, Maurizio</p><p>Glatzel, Markus</p><p>Gu, Yan</p><p>Guo, Jifeng</p><p>Guzman, Samuel</p><p>Han, Lei</p><p>Hawkins, Cynthia</p><p>Herms, Jochen</p><p>Highley, Robin</p><p>Horbinski, Craig</p><p>Irwin, David</p><p>Joseph, Jeffrey</p><p>Joutel, Anne</p><p>Kovacs, Gabor</p><p>Lammens, Martin</p><p>Langdon, Kristopher</p><p>Leske, Henning</p><p>Levine, Adrian</p><p>Li, Jianrong</p><p>Liu, Ying</p><p>Marklund, Niklas</p><p>Mechtler, Karl</p><p>Meinhardt, Jenny</p><p>Munoz, David</p><p>Nasrallah, MacLean</p><p>Nicolas, Gael</p><p>Nordin, Angelica</p><p>Piao, Yueshan</p><p>Pittella, José</p><p>Popa-Wagner, Aurel</p><p>Priller, Josef</p><p>Puig, Berta</p><p>Reimann, Jens</p><p>Rosi, Susanna</p><p>Rozemuller, Annemieke</p><p>Rushing, Elisabeth</p><p>Saleeb, Rola</p><p>Satomi, Kaishi</p><p>Schulz-Schaeffer, Walter J</p><p>Sepulveda-Falla, Diego</p><p>Shelkovnikova, Tatyana A</p><p>Springer, Wolfdieter</p><p>Tan, Jieqiong</p><p>Troakes, Claire</p><p>Vazquez-Manrique, Rafael</p><p>Vinters, Harry</p><p>Wakabayashi, Koichi</p><p>Wang, Yanjiang</p><p>Wang, Yu</p><p>Xu, Yuqiao</p><p>Yao, Yu</p><p>Zhao, Junli</p><p>Zheng, Danfeng</p><p>Zimmermann, Marina</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"34 1","pages":""},"PeriodicalIF":6.4,"publicationDate":"2023-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.13220","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138564797","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}
<p>A 63-year-old woman presented with a 2-month history of a rugged surface on the left parietal scalp. She reported slight pain when pressing the skin over the irregular area. Computed tomography (CT) showed mottling and small patchy destruction of the left parietal bone. Cranial contrast magnetic resonance imaging (MRI) revealed a homogeneously-enhanced, en plaque mass, measuring 59 × 22 mm. The MRI also showed that the mass had infiltrated the parietal bone, and the dural tail sign was present (Figure 1). Blood tests ruled out anemia (hemoglobin 10.6 g/dL), hypercalcemia (serum calcium: 2.25 mmol/L), and renal insufficiency (serum creatinine: 54 μmol/L). She denied having headaches, vomiting, epileptic seizures, and paresthesia. No other lesions were found during physical examination or imaging studies. On the basis of the radiological features of the lesion, en plaque meningioma was highly suspected, and the patient was advised to undergo tumor resection. Intraoperatively, the tumor was located in the epidural space and was completely resected via a left-sided parietal approach. The invaded bone was excised, and titanium mesh was used to restore the cranial bone defect. Postoperatively, the patient had no neurological deficits and was discharged on postoperative day 5 (Box 1).</p><p>Hematoxylin and eosin (H&E) staining showed a large number of cells with eccentrically located nuclei and prominent large nucleoli resembling plasma cells in the parietal lobe mass (Figure 2A). Immunohistochemical staining revealed tumor cells positive for cluster of differentiation (CD) 56 (Figure 2B), multiple myeloma oncogene 1 (MuM-1) (Figure 2C), lambda immunoglobulin light chains (Figure 2D), CD79a, but negative for side-to-side kappa immunoglobulin light chains (Figure 2E). The Ki-67 proliferation index was 15% (Figure 2F). In situ hybridization for Epstein–Barr virus encoded RNA was negative. Additionally, the tumor was negative for CD138, CD38, CD19, CD30, and cyclin D1 with immunohistochemical staining.</p><p>Plasma cell neoplasm.</p><p>The unexpected pathological diagnosis prompted a referral to hematology. In the hematology department, our patient underwent further evaluation, including urinalysis for Bence-Jones protein, PET, and bone marrow examination. The results of immunoglobulin testing were normal, and bone marrow examination revealed that the plasma cell percentage was 8.5%. Postoperative PET/CT revealed postoperative changes after resection of the left parietal tumor; no significant increase in glucose metabolism was observed in the whole-body images. All of above supported the diagnosis of plasmacytoma.</p><p>According to the International Consensus Classification of mature lymphoid neoplasms, plasmacytoma is defined as a localized neoplasm of clonal plasma cells without evidence of multiple myeloma. The diagnostic criteria are as follows: (1) biopsy-proven clonal plasma cell neoplasm of bone or extramedullary site; (2) no clonal B cells;
{"title":"A 63-year-old woman with parietal scalp surface rugged","authors":"Zhiwei Shen, Siqi Tao","doi":"10.1111/bpa.13224","DOIUrl":"10.1111/bpa.13224","url":null,"abstract":"<p>A 63-year-old woman presented with a 2-month history of a rugged surface on the left parietal scalp. She reported slight pain when pressing the skin over the irregular area. Computed tomography (CT) showed mottling and small patchy destruction of the left parietal bone. Cranial contrast magnetic resonance imaging (MRI) revealed a homogeneously-enhanced, en plaque mass, measuring 59 × 22 mm. The MRI also showed that the mass had infiltrated the parietal bone, and the dural tail sign was present (Figure 1). Blood tests ruled out anemia (hemoglobin 10.6 g/dL), hypercalcemia (serum calcium: 2.25 mmol/L), and renal insufficiency (serum creatinine: 54 μmol/L). She denied having headaches, vomiting, epileptic seizures, and paresthesia. No other lesions were found during physical examination or imaging studies. On the basis of the radiological features of the lesion, en plaque meningioma was highly suspected, and the patient was advised to undergo tumor resection. Intraoperatively, the tumor was located in the epidural space and was completely resected via a left-sided parietal approach. The invaded bone was excised, and titanium mesh was used to restore the cranial bone defect. Postoperatively, the patient had no neurological deficits and was discharged on postoperative day 5 (Box 1).</p><p>Hematoxylin and eosin (H&E) staining showed a large number of cells with eccentrically located nuclei and prominent large nucleoli resembling plasma cells in the parietal lobe mass (Figure 2A). Immunohistochemical staining revealed tumor cells positive for cluster of differentiation (CD) 56 (Figure 2B), multiple myeloma oncogene 1 (MuM-1) (Figure 2C), lambda immunoglobulin light chains (Figure 2D), CD79a, but negative for side-to-side kappa immunoglobulin light chains (Figure 2E). The Ki-67 proliferation index was 15% (Figure 2F). In situ hybridization for Epstein–Barr virus encoded RNA was negative. Additionally, the tumor was negative for CD138, CD38, CD19, CD30, and cyclin D1 with immunohistochemical staining.</p><p>Plasma cell neoplasm.</p><p>The unexpected pathological diagnosis prompted a referral to hematology. In the hematology department, our patient underwent further evaluation, including urinalysis for Bence-Jones protein, PET, and bone marrow examination. The results of immunoglobulin testing were normal, and bone marrow examination revealed that the plasma cell percentage was 8.5%. Postoperative PET/CT revealed postoperative changes after resection of the left parietal tumor; no significant increase in glucose metabolism was observed in the whole-body images. All of above supported the diagnosis of plasmacytoma.</p><p>According to the International Consensus Classification of mature lymphoid neoplasms, plasmacytoma is defined as a localized neoplasm of clonal plasma cells without evidence of multiple myeloma. The diagnostic criteria are as follows: (1) biopsy-proven clonal plasma cell neoplasm of bone or extramedullary site; (2) no clonal B cells;","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"34 2","pages":""},"PeriodicalIF":6.4,"publicationDate":"2023-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.13224","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138497903","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}
Kai Schmid, Jannik Sehring, Attila Németh, Patrick N. Harter, Katharina J. Weber, Abishaa Vengadeswaran, Holger Storf, Christian Seidemann, Kapil Karki, Patrick Fischer, Hildegard Dohmen, Carmen Selignow, Andreas von Deimling, Stefan Grau, Uwe Schröder, Karl H. Plate, Marco Stein, Eberhard Uhl, Till Acker, Daniel Amsel
The current state-of-the-art analysis of central nervous system (CNS) tumors through DNA methylation profiling relies on the tumor classifier developed by Capper and colleagues, which centrally harnesses DNA methylation data provided by users. Here, we present a distributed-computing-based approach for CNS tumor classification that achieves a comparable performance to centralized systems while safeguarding privacy. We utilize the t-distributed neighborhood embedding (t-SNE) model for dimensionality reduction and visualization of tumor classification results in two-dimensional graphs in a distributed approach across multiple sites (DistSNE). DistSNE provides an intuitive web interface (https://gin-tsne.med.uni-giessen.de) for user-friendly local data management and federated methylome-based tumor classification calculations for multiple collaborators in a DataSHIELD environment. The freely accessible web interface supports convenient data upload, result review, and summary report generation. Importantly, increasing sample size as achieved through distributed access to additional datasets allows DistSNE to improve cluster analysis and enhance predictive power. Collectively, DistSNE enables a simple and fast classification of CNS tumors using large-scale methylation data from distributed sources, while maintaining the privacy and allowing easy and flexible network expansion to other institutes. This approach holds great potential for advancing human brain tumor classification and fostering collaborative precision medicine in neuro-oncology.
{"title":"DistSNE: Distributed computing and online visualization of DNA methylation-based central nervous system tumor classification","authors":"Kai Schmid, Jannik Sehring, Attila Németh, Patrick N. Harter, Katharina J. Weber, Abishaa Vengadeswaran, Holger Storf, Christian Seidemann, Kapil Karki, Patrick Fischer, Hildegard Dohmen, Carmen Selignow, Andreas von Deimling, Stefan Grau, Uwe Schröder, Karl H. Plate, Marco Stein, Eberhard Uhl, Till Acker, Daniel Amsel","doi":"10.1111/bpa.13228","DOIUrl":"10.1111/bpa.13228","url":null,"abstract":"<p>The current state-of-the-art analysis of central nervous system (CNS) tumors through DNA methylation profiling relies on the tumor classifier developed by Capper and colleagues, which centrally harnesses DNA methylation data provided by users. Here, we present a distributed-computing-based approach for CNS tumor classification that achieves a comparable performance to centralized systems while safeguarding privacy. We utilize the t-distributed neighborhood embedding (t-SNE) model for dimensionality reduction and visualization of tumor classification results in two-dimensional graphs in a distributed approach across multiple sites (DistSNE). DistSNE provides an intuitive web interface (https://gin-tsne.med.uni-giessen.de) for user-friendly local data management and federated methylome-based tumor classification calculations for multiple collaborators in a DataSHIELD environment. The freely accessible web interface supports convenient data upload, result review, and summary report generation. Importantly, increasing sample size as achieved through distributed access to additional datasets allows DistSNE to improve cluster analysis and enhance predictive power. Collectively, DistSNE enables a simple and fast classification of CNS tumors using large-scale methylation data from distributed sources, while maintaining the privacy and allowing easy and flexible network expansion to other institutes. This approach holds great potential for advancing human brain tumor classification and fostering collaborative precision medicine in neuro-oncology.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"34 3","pages":""},"PeriodicalIF":6.4,"publicationDate":"2023-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.13228","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138443960","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}
Paula Merino-Serrais, Sergio Plaza-Alonso, Farida Hellal, Susana Valero-Freitag, Asta Kastanauskaite, Nikolaus Plesnila, Javier DeFelipe
Significant progress has been made with regard to understanding how the adult brain responds after a stroke. However, a large number of patients continue to suffer lifelong disabilities without adequate treatment. In the present study, we have analyzed possible microanatomical alterations in the contralesional hippocampus from the ischemic stroke mouse model tMCAo 12–14 weeks after transient middle cerebral artery occlusion. After individually injecting Lucifer yellow into pyramidal neurons from the CA1 field of the hippocampus, we performed a detailed three-dimensional analysis of the neuronal complexity, dendritic spine density, and morphology. We found that, in both apical (stratum radiatum) and basal (stratum oriens) arbors, CA1 pyramidal neurons in the contralesional hippocampus of tMCAo mice have a significantly higher neuronal complexity, as well as reduced spine density and alterations in spine volume and spine length. Our results show that when the ipsilateral hippocampus is dramatically damaged, the contralesional hippocampus exhibits several statistically significant selective alterations. However, these alterations are not as significant as expected, which may help to explain the recovery of hippocampal function after stroke. Further anatomical and physiological studies are necessary to better understand the modifications in the “intact” contralesional lesioned brain regions, which are probably fundamental to recover functions after stroke.
{"title":"Structural changes of CA1 pyramidal neurons after stroke in the contralesional hippocampus","authors":"Paula Merino-Serrais, Sergio Plaza-Alonso, Farida Hellal, Susana Valero-Freitag, Asta Kastanauskaite, Nikolaus Plesnila, Javier DeFelipe","doi":"10.1111/bpa.13222","DOIUrl":"10.1111/bpa.13222","url":null,"abstract":"<p>Significant progress has been made with regard to understanding how the adult brain responds after a stroke. However, a large number of patients continue to suffer lifelong disabilities without adequate treatment. In the present study, we have analyzed possible microanatomical alterations in the contralesional hippocampus from the ischemic stroke mouse model tMCAo 12–14 weeks after transient middle cerebral artery occlusion. After individually injecting Lucifer yellow into pyramidal neurons from the CA1 field of the hippocampus, we performed a detailed three-dimensional analysis of the neuronal complexity, dendritic spine density, and morphology. We found that, in both apical (<i>stratum radiatum</i>) and basal (<i>stratum oriens</i>) arbors, CA1 pyramidal neurons in the contralesional hippocampus of tMCAo mice have a significantly higher neuronal complexity, as well as reduced spine density and alterations in spine volume and spine length. Our results show that when the ipsilateral hippocampus is dramatically damaged, the contralesional hippocampus exhibits several statistically significant selective alterations. However, these alterations are not as significant as expected, which may help to explain the recovery of hippocampal function after stroke. Further anatomical and physiological studies are necessary to better understand the modifications in the “intact” contralesional lesioned brain regions, which are probably fundamental to recover functions after stroke.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"34 3","pages":""},"PeriodicalIF":6.4,"publicationDate":"2023-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.13222","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138443963","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}
Yan Cao, Pan Liu, Hongfei Bian, Sixuan Jin, Jiaqi Liu, Ning Yu, Huan Cui, Fengrun Sun, Xiaojing Qian, Wenying Qiu, Chao Ma
Adult hippocampal neurogenesis (AHN), essential for the plasticity of hippocampal structure and function, may be disrupted in Alzheimer‘s disease (AD). However, the relationship between the changes in AHN and AD-related pathology in humans remains uncertain. By utilizing advanced immunostaining techniques, we could identify multiple biomarkers representing different stages of AHN in postmortem human hippocampal tissue that exhibited various AD-related neuropathological changes. In this study, we observed a significant presence of neurogenic cells in the hippocampus's dentate gyrus (DG) region in 30 individuals, including 14 individuals diagnosed with AD-related neuropathological changes and the remaining 16 individuals without any neurological diseases. Further investigation revealed that patients with AD exhibited pronounced astrogliosis and reduced neurogenesis. Specifically, the number of neuroblasts, immature and early mature granule cells decreased significantly as AD advanced. Although the number of neural stem cells (NSCs) remained unchanged in AD patients compared with mentally healthy individuals, they tended to be more quiescent state regulated by Notch and bone morphogenetic protein (BMP) signaling pathways. These abnormalities were strongly associated with the neuropathological alterations in AD patients. These research findings provide potential insights into the underlying mechanisms that underpin the pathogenesis of AD.
{"title":"Reduced neurogenesis in human hippocampus with Alzheimer's disease","authors":"Yan Cao, Pan Liu, Hongfei Bian, Sixuan Jin, Jiaqi Liu, Ning Yu, Huan Cui, Fengrun Sun, Xiaojing Qian, Wenying Qiu, Chao Ma","doi":"10.1111/bpa.13225","DOIUrl":"10.1111/bpa.13225","url":null,"abstract":"<p>Adult hippocampal neurogenesis (AHN), essential for the plasticity of hippocampal structure and function, may be disrupted in Alzheimer‘s disease (AD). However, the relationship between the changes in AHN and AD-related pathology in humans remains uncertain. By utilizing advanced immunostaining techniques, we could identify multiple biomarkers representing different stages of AHN in postmortem human hippocampal tissue that exhibited various AD-related neuropathological changes. In this study, we observed a significant presence of neurogenic cells in the hippocampus's dentate gyrus (DG) region in 30 individuals, including 14 individuals diagnosed with AD-related neuropathological changes and the remaining 16 individuals without any neurological diseases. Further investigation revealed that patients with AD exhibited pronounced astrogliosis and reduced neurogenesis. Specifically, the number of neuroblasts, immature and early mature granule cells decreased significantly as AD advanced. Although the number of neural stem cells (NSCs) remained unchanged in AD patients compared with mentally healthy individuals, they tended to be more quiescent state regulated by Notch and bone morphogenetic protein (BMP) signaling pathways. These abnormalities were strongly associated with the neuropathological alterations in AD patients. These research findings provide potential insights into the underlying mechanisms that underpin the pathogenesis of AD.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"34 3","pages":""},"PeriodicalIF":6.4,"publicationDate":"2023-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.13225","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138443962","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}
Matthew D. Cykowski, Anithachristy S. Arumanayagam, Suzanne Z. Powell, Stanley H. Appel
Poly-GA and poly-GP immunofluorescence studies show conspicuous dipeptide repeat pathology in layers IV and II of primary visual cortex in C9ALS patients.
{"title":"Primary visual cortex pathology in ALS patients with C9ORF72 expansion","authors":"Matthew D. Cykowski, Anithachristy S. Arumanayagam, Suzanne Z. Powell, Stanley H. Appel","doi":"10.1111/bpa.13229","DOIUrl":"10.1111/bpa.13229","url":null,"abstract":"<p>Poly-GA and poly-GP immunofluorescence studies show conspicuous dipeptide repeat pathology in layers IV and II of primary visual cortex in C9ALS patients.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"34 5","pages":""},"PeriodicalIF":5.8,"publicationDate":"2023-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.13229","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138443961","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}
Emmanuelle Uro-Coste, Arnault Tauziede-Espariat, Charlotte Dubucs, Dan Christian Chiforeanu, Aurore Siegfried, Yvan Nicaise, Luc Bauchet, Laurent Riffaud, Franck Bielle, Alexandre Vasiljevic, Romain Appay, Solène Evrard, Pascale Varlet, Valérie Rigau, The Biopathology RENOCLIP-LOC network
We report here about two novel tumours classified as extraventricular neurocytomas (EVN) using DNA-methylation profiling, associated with NTRK2 fusions instead of the usual FGFR1 alterations so far attributed to this tumoural entity. We present the second detailed case of an intraventricular presentation in the MC EVN. Our findings broaden the spectrum of MC EVN and have implications in terms of diagnosis, therapy and terminology.
{"title":"Two novel tumours with NTRK2 fusion in the methylation class of extraventricular neurocytomas, including one intraventricular","authors":"Emmanuelle Uro-Coste, Arnault Tauziede-Espariat, Charlotte Dubucs, Dan Christian Chiforeanu, Aurore Siegfried, Yvan Nicaise, Luc Bauchet, Laurent Riffaud, Franck Bielle, Alexandre Vasiljevic, Romain Appay, Solène Evrard, Pascale Varlet, Valérie Rigau, The Biopathology RENOCLIP-LOC network","doi":"10.1111/bpa.13223","DOIUrl":"10.1111/bpa.13223","url":null,"abstract":"<p>We report here about two novel tumours classified as extraventricular neurocytomas (EVN) using DNA-methylation profiling, associated with NTRK2 fusions instead of the usual FGFR1 alterations so far attributed to this tumoural entity. We present the second detailed case of an intraventricular presentation in the MC EVN. Our findings broaden the spectrum of MC EVN and have implications in terms of diagnosis, therapy and terminology.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"34 3","pages":""},"PeriodicalIF":6.4,"publicationDate":"2023-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.13223","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138294705","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}
Takashi Ando, Yuichi Riku, Akio Akagi, Hiroaki Miyahara, Takashi Uematsu, Ikuko Aiba, Jun Sone, Masahisa Katsuno, Mari Yoshida, Yasushi Iwasaki
Multiple system atrophy (MSA) is an adult-onset neurodegenerative disorder that presents with variable combinations of autonomic dysfunction, cerebellar ataxia, parkinsonism, and pyramidal signs. The inferior olivary nucleus is targeted in MSA, with a phenotype of olivopontocerebellar atrophy in particular, and involvement of the olivocerebellar tract is well known. However, degeneration of the olivospinal tract has not been studied in MSA. We examined 97 spinal cords from consecutively autopsied patients with MSA. Myelin staining revealed that 22 cords (22.7%) had small, bilateral, triangular-shaped tract degeneration in the boundary of the anterior and lateral funiculi, which appeared continuously from C1 to C5. The anatomical pathway of the degenerated tract was consistent with the description of the olivospinal tract provided by Helweg in 1888. The MSA patients showing degeneration of this tract were younger at disease onset (average: 56.4 ± 8.7 years, range: 42–74), and had longer disease duration (average: 10.1 ± 4.8 years, range: 2–25) and more severe olivopontocerebellar changes compared to other MSA patients. Quantitative analyses revealed that patients with olivospinal tract degeneration had a lower neuronal density in the inferior olivary nucleus compared to other patients. Microglial density in this tract was negatively correlated with the neuronal density in the inferior olivary nucleus. The densities of glial cytoplasmic inclusions in the inferior olivary nucleus and in the olivospinal tract were strongly correlated with each other. Neurologically healthy controls (n = 22) and disease controls with Lewy body disease (n = 30), amyotrophic lateral sclerosis (n = 30), and progressive supranuclear palsy (n = 30) did not present the olivospinal tract degeneration. Our results indicate an impairment of the neural connection between the inferior olivary nucleus and the spinal cord in MSA patients, which may develop in a descending manner.
{"title":"Degeneration of olivospinal tract in the upper cervical spinal cord of multiple system atrophy patients: Reappraisal of Helweg's triangular tract","authors":"Takashi Ando, Yuichi Riku, Akio Akagi, Hiroaki Miyahara, Takashi Uematsu, Ikuko Aiba, Jun Sone, Masahisa Katsuno, Mari Yoshida, Yasushi Iwasaki","doi":"10.1111/bpa.13226","DOIUrl":"10.1111/bpa.13226","url":null,"abstract":"<p>Multiple system atrophy (MSA) is an adult-onset neurodegenerative disorder that presents with variable combinations of autonomic dysfunction, cerebellar ataxia, parkinsonism, and pyramidal signs. The inferior olivary nucleus is targeted in MSA, with a phenotype of olivopontocerebellar atrophy in particular, and involvement of the olivocerebellar tract is well known. However, degeneration of the olivospinal tract has not been studied in MSA. We examined 97 spinal cords from consecutively autopsied patients with MSA. Myelin staining revealed that 22 cords (22.7%) had small, bilateral, triangular-shaped tract degeneration in the boundary of the anterior and lateral funiculi, which appeared continuously from C1 to C5. The anatomical pathway of the degenerated tract was consistent with the description of the olivospinal tract provided by Helweg in 1888. The MSA patients showing degeneration of this tract were younger at disease onset (average: 56.4 ± 8.7 years, range: 42–74), and had longer disease duration (average: 10.1 ± 4.8 years, range: 2–25) and more severe olivopontocerebellar changes compared to other MSA patients. Quantitative analyses revealed that patients with olivospinal tract degeneration had a lower neuronal density in the inferior olivary nucleus compared to other patients. Microglial density in this tract was negatively correlated with the neuronal density in the inferior olivary nucleus. The densities of glial cytoplasmic inclusions in the inferior olivary nucleus and in the olivospinal tract were strongly correlated with each other. Neurologically healthy controls (<i>n</i> = 22) and disease controls with Lewy body disease (<i>n</i> = 30), amyotrophic lateral sclerosis (<i>n</i> = 30), and progressive supranuclear palsy (<i>n</i> = 30) did not present the olivospinal tract degeneration. Our results indicate an impairment of the neural connection between the inferior olivary nucleus and the spinal cord in MSA patients, which may develop in a descending manner.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"34 3","pages":""},"PeriodicalIF":6.4,"publicationDate":"2023-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.13226","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136396465","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}
Stefan Gingele, Thiemo M. Möllenkamp, Florian Henkel, Lara-Jasmin Schröder, Martin W. Hümmert, Thomas Skripuletz, Martin Stangel, Viktoria Gudi
Multiple sclerosis is a chronic autoimmune disease of the central nervous system characterized by myelin loss, axonal damage, and glial scar formation. Still, the underlying processes remain unclear, as numerous pathways and factors have been found to be involved in the development and progression of the disease. Therefore, it is of great importance to find suitable animal models as well as reliable methods for their precise and reproducible analysis. Here, we describe the impact of demyelination on clinically relevant gray matter regions of the hippocampus and cerebral cortex, using the previously established cuprizone model for aged mice. We could show that bioinformatic image analysis methods are not only suitable for quantification of cell populations, but also for the assessment of de- and remyelination processes, as numerous objective parameters can be considered for reproducible measurements. After cuprizone-induced demyelination, subsequent remyelination proceeded slowly and remained incomplete in all gray matter areas studied. There were regional differences in the number of mature oligodendrocytes during remyelination suggesting region-specific differences in the factors accounting for remyelination failure, as, even in the presence of oligodendrocytes, remyelination in the cortex was found to be impaired. Upon cuprizone administration, synaptic density and dendritic volume in the gray matter of aged mice decreased. The intensity of synaptophysin staining gradually restored during the subsequent remyelination phase, however the expression of MAP2 did not fully recover. Microgliosis persisted in the gray matter of aged animals throughout the remyelination period, whereas extensive astrogliosis was of short duration as compared to white matter structures. In conclusion, we demonstrate that the application of the cuprizone model in aged mice mimics the impaired regeneration ability seen in human pathogenesis more accurately than commonly used protocols with young mice and therefore provides an urgently needed animal model for the investigation of remyelination failure and remyelination-enhancing therapies.
{"title":"Automated analysis of gray matter damage in aged mice reveals impaired remyelination in the cuprizone model","authors":"Stefan Gingele, Thiemo M. Möllenkamp, Florian Henkel, Lara-Jasmin Schröder, Martin W. Hümmert, Thomas Skripuletz, Martin Stangel, Viktoria Gudi","doi":"10.1111/bpa.13218","DOIUrl":"10.1111/bpa.13218","url":null,"abstract":"<p>Multiple sclerosis is a chronic autoimmune disease of the central nervous system characterized by myelin loss, axonal damage, and glial scar formation. Still, the underlying processes remain unclear, as numerous pathways and factors have been found to be involved in the development and progression of the disease. Therefore, it is of great importance to find suitable animal models as well as reliable methods for their precise and reproducible analysis. Here, we describe the impact of demyelination on clinically relevant gray matter regions of the hippocampus and cerebral cortex, using the previously established cuprizone model for aged mice. We could show that bioinformatic image analysis methods are not only suitable for quantification of cell populations, but also for the assessment of de- and remyelination processes, as numerous objective parameters can be considered for reproducible measurements. After cuprizone-induced demyelination, subsequent remyelination proceeded slowly and remained incomplete in all gray matter areas studied. There were regional differences in the number of mature oligodendrocytes during remyelination suggesting region-specific differences in the factors accounting for remyelination failure, as, even in the presence of oligodendrocytes, remyelination in the cortex was found to be impaired. Upon cuprizone administration, synaptic density and dendritic volume in the gray matter of aged mice decreased. The intensity of synaptophysin staining gradually restored during the subsequent remyelination phase, however the expression of MAP2 did not fully recover. Microgliosis persisted in the gray matter of aged animals throughout the remyelination period, whereas extensive astrogliosis was of short duration as compared to white matter structures. In conclusion, we demonstrate that the application of the cuprizone model in aged mice mimics the impaired regeneration ability seen in human pathogenesis more accurately than commonly used protocols with young mice and therefore provides an urgently needed animal model for the investigation of remyelination failure and remyelination-enhancing therapies.</p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"34 2","pages":""},"PeriodicalIF":6.4,"publicationDate":"2023-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.13218","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71478265","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}
Christopher Kobylecki, Jennifer C. Thompson, Andrew C. Robinson, Federico Roncaroli, Julie S. Snowden, David M. Mann
A 70-year-old man presented to the clinic with impairment of visual memory and marked predominantly right sided mesial temporal lobe atrophy on imaging. He died 6 years following symptom onset and neuropathological examination showed concomitant progressive supranuclear palsy and Lewy body pathology. Although he did not fulfil clinical criteria for either condition at presentation, we propose that interactions between the two pathologies in mesial temporal regions could result in this atypical clinical phenotype.
{"title":"Concomitant progressive supranuclear palsy and Lewy body pathology presenting with circumscribed visual memory loss: A clinicopathological case","authors":"Christopher Kobylecki, Jennifer C. Thompson, Andrew C. Robinson, Federico Roncaroli, Julie S. Snowden, David M. Mann","doi":"10.1111/bpa.13219","DOIUrl":"10.1111/bpa.13219","url":null,"abstract":"<p>A 70-year-old man presented to the clinic with impairment of visual memory and marked predominantly right sided mesial temporal lobe atrophy on imaging. He died 6 years following symptom onset and neuropathological examination showed concomitant progressive supranuclear palsy and Lewy body pathology. Although he did not fulfil clinical criteria for either condition at presentation, we propose that interactions between the two pathologies in mesial temporal regions could result in this atypical clinical phenotype.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":9290,"journal":{"name":"Brain Pathology","volume":"34 4","pages":""},"PeriodicalIF":5.8,"publicationDate":"2023-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bpa.13219","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71478266","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}
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