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CNS-associated macrophages contribute to intracerebral aneurysm pathophysiology Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-03-18 Martina Glavan, Ana Jelic, Damien Levard, Juhana Frösen, Sara Keränen, Bart A. A. Franx, Ana-Rita Bras, Estelle R. Louet, Ádám Dénes, Mario Merlini, Denis Vivien, Marina Rubio
Intracerebral aneurysms (IAs) are pathological dilatations of cerebral arteries whose rupture leads to subarachnoid hemorrhage, a significant cause of disability and death. Inflammation is recognized as a critical contributor to the formation, growth, and rupture of IAs; however, its precise actors have not yet been fully elucidated. Here, we report CNS-associated macrophages (CAMs), also known as
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Molecular and clinicopathologic characteristics of CNS embryonal tumors with BRD4::LEUTX fusion Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-03-18 Felipe Andreiuolo, Christina K. Ferrone, Sharika Rajan, Arie Perry, Ekin Guney, Elaine Cham, Caterina Giannini, Angus Toland, Nicholas Willard, Andrea Silveira de Souza, Karen Dazelle, Hye-Jung Chung, Omkar Singh, Kyle Conway, Nicholas Coley, Christopher Dampier, Zied Abdullaev, Drew Pratt, Patrick J. Cimino, Martha Quezado, Kenneth Aldape
Central nervous system (CNS) embryonal tumors are a heterogeneous group of high-grade malignancies, and the increasing clinical use of methylation profiling and next-generation sequencing has led to the identification of molecularly distinct subtypes. One proposed tumor type, CNS tumor with BRD4::LEUTX fusion, has been described. As only a few CNS tumors with BRD4::LEUTX fusions have been described
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Beyond genetics: including the environmental dimension in amyloidosis mouse models for Alzheimer’s disease Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-03-18 Lien Van Hoecke, Roosmarijn E. Vandenbroucke
The prevalence of Alzheimer’s disease (AD) continues to increase, with projections estimating 70 million patients by 2030. While recent FDA approvals for Aducanumab and Lecanemab have generated optimism, these therapies offer only partial relief by slowing cognitive decline [1–2], leaving us ill-equipped to face the looming AD epidemic. To better address AD, we must enhance our understanding of its
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DNA hypomethylator phenotype reprograms glutamatergic network in receptor tyrosine kinase gene-mutated glioblastoma Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-03-13 Mio Harachi, Kenta Masui, Erika Shimizu, Kumiko Murakami, Hiromi Onizuka, Yoshihiro Muragaki, Takakazu Kawamata, Hisako Nakayama, Mariko Miyata, Takashi Komori, Webster K. Cavenee, Paul S. Mischel, Atsushi Kurata, Noriyuki Shibata
DNA methylation is crucial for chromatin structure and gene expression and its aberrancies, including the global “hypomethylator phenotype”, are associated with cancer. Here we show that an underlying mechanism for this phenotype in the large proportion of the highly lethal brain tumor glioblastoma (GBM) carrying receptor tyrosine kinase gene mutations, involves the mechanistic target of rapamycin
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Organelle resolved proteomics uncovers PLA2R1 as a novel cell surface marker required for chordoma growth Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-03-07 Shahbaz Khan, Jeffrey A. Zuccato, Vladimir Ignatchenko, Olivia Singh, Meinusha Govindarajan, Matthew Waas, Salvador Mejia-Guerrero, Andrew Gao, Gelareh Zadeh, Thomas Kislinger
Chordomas are clinically aggressive tumors with a high rate of disease progression despite maximal therapy. Given the limited therapeutic options available, there remains an urgent need for the development of novel therapies to improve clinical outcomes. Cell surface proteins are attractive therapeutic targets yet are challenging to profile with common methods. Four chordoma cell lines were analyzed
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Blood-based CNS regionally and neuronally enriched extracellular vesicles carrying pTau217 for Alzheimer’s disease diagnosis and differential diagnosis Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-03-05 Zhen Guo, Chen Tian, Yang Shi, Xue-Ru Song, Wei Yin, Qing-Qing Tao, Jie Liu, Guo-Ping Peng, Zhi-Ying Wu, Yan-Jiang Wang, Zhen-Xin Zhang, Jing Zhang
Accurate differential diagnosis among various dementias is crucial for effective treatment of Alzheimer’s disease (AD). The study began with searching for novel blood-based neuronal extracellular vesicles (EVs) that are more enriched in the brain regions vulnerable to AD development and progression. With extensive proteomic profiling, GABRD and GPR162 were identified as novel brain regionally enriched
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Prophylactic nicotinamide treatment protects from rotenone-induced neurodegeneration by increasing mitochondrial content and volume Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-03-01 Amin Otmani, Gauti Jóhannesson, Rune Brautaset, James R. Tribble, Pete A. Williams
Leber’s hereditary optic neuropathy (LHON) is driven by mtDNA mutations affecting Complex I presenting as progressive retinal ganglion cell dysfunction usually in the absence of extra-ophthalmic symptoms. There are no long-term neuroprotective agents for LHON. Oral nicotinamide provides a robust neuroprotective effect against mitochondrial and metabolic dysfunction in other retinal injuries. We explored
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Exploring the significance of caspase-cleaved tau in tauopathies and as a complementary pathology to phospho-tau in Alzheimer’s disease: implications for biomarker development and therapeutic targeting Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-28 Liara Rizzi, Lea T. Grinberg
Tauopathies are neurodegenerative diseases that typically require postmortem examination for a definitive diagnosis. Detecting neurotoxic tau fragments in cerebrospinal fluid (CSF) and serum provides an opportunity for in vivo diagnosis and disease monitoring. Current assays primarily focus on total tau or phospho-tau, overlooking other post-translational modifications (PTMs). Caspase-cleaved tau is
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Decoding of the surfaceome and endocytome in primary glioblastoma cells identifies potential target antigens in the hypoxic tumor niche Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-27 Kelin Gonçalves de Oliveira, Anna Bång-Rudenstam, Sarah Beyer, Axel Boukredine, Hugo Talbot, Valeria Governa, Maria C. Johansson, Ann-Sofie Månsson, Karin Forsberg-Nilsson, Johan Bengzon, Johan Malmström, Charlotte Welinder, Mattias Belting
Immunotherapies with antibody–drug-conjugates (ADC) and CAR-T cells, targeted at tumor surface antigens (surfaceome), currently revolutionize clinical oncology. However, target identification warrants a better understanding of the surfaceome and how it is modulated by the tumor microenvironment. Here, we decode the surfaceome and endocytome and its remodeling by hypoxic stress in glioblastoma (GBM)
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Astrocytic accumulation of tau fibrils isolated from Alzheimer’s disease brains induces inflammation, cell-to-cell propagation and neuronal impairment Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-26 Khalid Eltom, Tobias Mothes, Sylwia Libard, Martin Ingelsson, Anna Erlandsson
Accumulating evidence highlights the involvement of astrocytes in Alzheimer’s disease (AD) progression. We have previously demonstrated that human iPSC-derived astrocytes ingest and modify synthetic tau fibrils in a way that enhances their seeding efficiency. However, synthetic tau fibrils differ significantly from in vivo formed fibrils. To mimic the situation in the brain, we here analyzed astrocytes’
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CNS embryonal tumour with concomitant novel BRD4::CTRC1 fusion and BCOR internal tandem duplication – evidence for synergism and non-mutually exclusive alterations in CNS embryonal tumours Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-26 Sze Jet Aw, Enrica Ee Kar Tan, Sharon Yin Yee Low, Chik Hong Kuick, Jian Yuan Goh, Kenneth Tou En Chang
Central nervous system (CNS) embryonal tumours Not Elsewhere Classified/Not Otherwise Specified (NEC/NOS) is a category of CNS embryonal tumours lacking genetic alterations of a defined classification group. Recently, Lebrun et al. described a patient with a CNS embryonal tumour with a BRD4::LEUTX fusion, which matched the methylation profile of ‘CNS embryonal tumour with BRD4::LEUTX fusion’ using
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Stimulating VAPB-PTPIP51 ER-mitochondria tethering corrects FTD/ALS mutant TDP43 linked Ca2+ and synaptic defects Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-23 Andrea Markovinovic, Sandra M. Martín-Guerrero, Gábor M. Mórotz, Shaakir Salam, Patricia Gomez-Suaga, Sebastien Paillusson, Jenny Greig, Younbok Lee, Jacqueline C. Mitchell, Wendy Noble, Christopher C.J. Miller
Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are clinically linked major neurodegenerative diseases. Notably, TAR DNA-binding protein-43 (TDP43) accumulations are hallmark pathologies of FTD/ALS and mutations in the gene encoding TDP43 cause familial FTD/ALS. There are no cures for FTD/ALS. FTD/ALS display damage to a broad range of physiological functions, many of which are
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Phenotypically concordant distribution of pick bodies in aphasic versus behavioral dementias Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-22 Allegra Kawles, Rachel Keszycki, Grace Minogue, Antonia Zouridakis, Ivan Ayala, Nathan Gill, Alyssa Macomber, Vivienne Lubbat, Christina Coventry, Emily Rogalski, Sandra Weintraub, Qinwen Mao, Margaret E. Flanagan, Hui Zhang, Rudolph Castellani, Eileen H. Bigio, M.-Marsel Mesulam, Changiz Geula, Tamar Gefen
Pick’s disease (PiD) is a subtype of the tauopathy form of frontotemporal lobar degeneration (FTLD-tau) characterized by intraneuronal 3R-tau inclusions. PiD can underly various dementia syndromes, including primary progressive aphasia (PPA), characterized by an isolated and progressive impairment of language and left-predominant atrophy, and behavioral variant frontotemporal dementia (bvFTD), characterized
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The cycad genotoxin methylazoxymethanol, linked to Guam ALS/PDC, induces transcriptional mutagenesis Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-21 Bert M. Verheijen, Claire Chung, Ben Thompson, Hyunjin Kim, Asa Nakahara, Jasper J. Anink, James D. Mills, Jeong H. Lee, Eleonora Aronica, Kiyomitsu Oyanagi, Akiyoshi Kakita, Jean-Francois Gout, Marc Vermulst
Guam amyotrophic lateral sclerosis/parkinsonism–dementia complex (ALS/PDC) is a rare neurodegenerative disorder with high prevalence among the native Chamorro population of Guam (Mariana Islands) [1,2,3]. ALS/PDC presents clinically as progressive motor neuron disease (resembling classic ALS), parkinsonism with dementia, or a combination of both. At the neuropathological level, ALS/PDC is characterized
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Hippocampal capillary pericytes in post-stroke and vascular dementias and Alzheimer’s disease and experimental chronic cerebral hypoperfusion Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-15 Yoshiki Hase, Dan Jobson, Jeremy Cheong, Kelvin Gotama, Luciana Maffei, Mai Hase, Alhafidz Hamdan, Ren Ding, Tuomo Polivkoski, Karen Horsburgh, Raj N. Kalaria
Neurovascular unit mural cells called ‘pericytes’ maintain the blood-brain barrier and local cerebral blood flow. Pathological changes in the hippocampus predispose to cognitive impairment and dementia. The role of hippocampal pericytes in dementia is largely unknown. We investigated hippocampal pericytes in 90 post-mortem brains from post-stroke dementia (PSD), vascular dementia (VaD), Alzheimer’s
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Prevalence, distribution, and severity of cerebral amyloid angiopathy differ between Lewy body diseases and Alzheimer’s disease Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-15 Lauren Walker, Harry Simpson, Alan J. Thomas, Johannes Attems
Dementia with Lewy bodies (DLB), Parkinson’s disease dementia (PDD), and Parkinson’s disease (PD) collectively known as Lewy body diseases (LBDs) are neuropathologically characterised by α-synuclein deposits (Lewy bodies and Lewy neurites). However, LBDs also exhibit pathology associated with Alzheimer’s disease (AD) (i.e. hyperphosphorylated tau and amyloid β (Aβ). Aβ can be deposited in the walls
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Correction to: Mild traumatic brain injury induces microvascular injury and accelerates Alzheimer-like pathogenesis in mice Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-15 Yingxi Wu, Haijian Wu, Jianxiong Zeng, Brock Pluimer, Shirley Dong, Xiaochun Xie, Xinying Guo, Tenghuan Ge, Xinyan Liang, Sudi Feng, Youzhen Yan, Jian‑Fu Chen, Naomi Sta Maria, Qingyi Ma, Fernando Gomez‑Pinilla, Zhen Zhao
Correction to: Acta neuropathol commun 9, 74(2021) https://doi.org/10.1186/s40478-021-01178-7 Following publication of the original article [1], the authors identified errors in Fig. 4; the two images of the dentate gyrus (DG) in Fig. 4a, and two images of CA1 in Fig. 4b. We have determined that there is a high degree of similarities between these images. After we located the original confocal scans
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Correction: Lesion of the subiculum reduces the spread of amyloid beta pathology to interconnected brain regions in a mouse model of Alzheimer’s disease Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-14 Sonia George, Annica Rönnbäck, Gunnar K. Gouras, Géraldine H. Petit, Fiona Grueninger, Bengt Winblad, Caroline Graff, Patrik Brundin
Correction: Acta Neuropathol Commun 2, 17 (2014) https://doi.org/10.1186/2051-5960-2-17 Following publication of the original article [1], the authors identified an error in Fig. 2b. The correct figure and caption is given below. Two panels in figure 2b were images captured from the same mouse by error and have been removed. Accessing the original data is not possible, as the files no longer exist
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Impact of APOE on amyloid and tau accumulation in argyrophilic grain disease and Alzheimer’s disease Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-09 Ana-Caroline Raulin, Sydney V. Doss, Michael G. Heckman, Emily C. Craver, Zonghua Li, Tadafumi C. Ikezu, Hiroaki Sekiya, Chia-Chen Liu, Yuka A. Martens, Cassandra L. Rosenberg, Lindsey A. Kuchenbecker, Michael DeTure, R. Ross Reichard, Aivi T. Nguyen, Eleni Constantopoulos, Rachel A. Larsen, Emmaline K. Kounaves, Melissa E. Murray, Dennis W. Dickson, Ronald C. Petersen, Guojun Bu, Takahisa Kanekiyo
Alzheimer’s disease (AD), characterized by the deposition of amyloid-β (Aβ) in senile plaques and neurofibrillary tangles of phosphorylated tau (pTau), is increasingly recognized as a complex disease with multiple pathologies. AD sometimes pathologically overlaps with age-related tauopathies such as four repeat (4R)-tau predominant argyrophilic grain disease (AGD). While AGD is often detected with
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The Schwann cell-specific G-protein Gαo (Gnao1) is a cell-intrinsic controller contributing to the regulation of myelination in peripheral nerve system Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-08 Jinghui Xu, Qianqian Peng, Jieyi Cai, Jianghong Shangguan, Wenfeng Su, Gang Chen, Hualin Sun, Changlai Zhu, Yun Gu
Myelin sheath abnormality is the cause of various neurodegenerative diseases (NDDs). G-proteins and their coupled receptors (GPCRs) play the important roles in myelination. Gnao1, encoding the major Gα protein (Gαo) in mammalian nerve system, is required for normal motor function. Here, we show that Gnao1 restricted to Schwann cell (SCs) lineage, but not neurons, negatively regulate SC differentiation
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Loss of Sarm1 reduces retinal ganglion cell loss in chronic glaucoma Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-08 Huilan Zeng, Jordan E. Mayberry, David Wadkins, Nathan Chen, Daniel W. Summers, Markus H. Kuehn
Glaucoma is one of the leading causes of irreversible blindness worldwide and vision loss in the disease results from the deterioration of retinal ganglion cells (RGC) and their axons. Metabolic dysfunction of RGC plays a significant role in the onset and progression of the disease in both human patients and rodent models, highlighting the need to better define the mechanisms regulating cellular energy
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Altered amyloid-β structure markedly reduces gliosis in the brain of mice harboring the Uppsala APP deletion Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-05 María Pagnon de la Vega, Stina Syvänen, Vilmantas Giedraitis, Monique Hooley, Evangelos Konstantinidis, Silvio R. Meier, Johanna Rokka, Jonas Eriksson, Ximena Aguilar, Tara L. Spires-Jones, Lars Lannfelt, Lars N. G. Nilsson, Anna Erlandsson, Greta Hultqvist, Martin Ingelsson, Dag Sehlin
Deposition of amyloid beta (Aβ) into plaques is a major hallmark of Alzheimer’s disease (AD). Different amyloid precursor protein (APP) mutations cause early-onset AD by altering the production or aggregation properties of Aβ. We recently identified the Uppsala APP mutation (APPUpp), which causes Aβ pathology by a triple mechanism: increased β-secretase and altered α-secretase APP cleavage, leading
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Dysregulation of stress granule dynamics by DCTN1 deficiency exacerbates TDP-43 pathology in Drosophila models of ALS/FTD Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-04 Tetsuhiro Ueda, Toshihide Takeuchi, Nobuhiro Fujikake, Mari Suzuki, Eiko N. Minakawa, Morio Ueyama, Yuzo Fujino, Nobuyuki Kimura, Seiichi Nagano, Akio Yokoseki, Osamu Onodera, Hideki Mochizuki, Toshiki Mizuno, Keiji Wada, Yoshitaka Nagai
The abnormal aggregation of TDP-43 into cytoplasmic inclusions in affected neurons is a major pathological hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Although TDP-43 is aberrantly accumulated in the neurons of most patients with sporadic ALS/FTD and other TDP-43 proteinopathies, how TDP-43 forms cytoplasmic aggregates remains unknown. In this study, we show that
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Brain injury drives optic glioma formation through neuron-glia signaling Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-02 Jit Chatterjee, Joshua P. Koleske, Astoria Chao, Andrew D. Sauerbeck, Ji-Kang Chen, Xuanhe Qi, Megan Ouyang, Lucy G. Boggs, Rujuta Idate, Lara Isabel Marco Y Marquez, Terrence T. Kummer, David H. Gutmann
Tissue injury and tumorigenesis share many cellular and molecular features, including immune cell (T cells, monocytes) infiltration and inflammatory factor (cytokines, chemokines) elaboration. Their common pathobiology raises the intriguing possibility that brain injury could create a tissue microenvironment permissive for tumor formation. Leveraging several murine models of the Neurofibromatosis type
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Early inner plexiform layer thinning and retinal nerve fiber layer thickening in excitotoxic retinal injury using deep learning-assisted optical coherence tomography Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-02-01 Da Ma, Wenyu Deng, Zain Khera, Thajunnisa A. Sajitha, Xinlei Wang, Gadi Wollstein, Joel S. Schuman, Sieun Lee, Haolun Shi, Myeong Jin Ju, Joanne Matsubara, Mirza Faisal Beg, Marinko Sarunic, Rebecca M. Sappington, Kevin C. Chan
Excitotoxicity from the impairment of glutamate uptake constitutes an important mechanism in neurodegenerative diseases such as Alzheimer’s, multiple sclerosis, and Parkinson's disease. Within the eye, excitotoxicity is thought to play a critical role in retinal ganglion cell death in glaucoma, diabetic retinopathy, retinal ischemia, and optic nerve injury, yet how excitotoxic injury impacts different
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Interplay between androgen and CXCR4 chemokine signaling in myelin repair Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-30 Narimène Asbelaoui, Charly Abi-Ghanem, Géraldine Schlecht-Louf, Hania Oukil, Michael Schumacher, Abdel Mouman Ghoumari
In men, reduced levels of testosterone are associated with the prevalence and progression of multiple sclerosis (MS), a chronic and disabling demyelinating disorder. Testosterone has been shown to promote myelin repair. Here, we demonstrate that the cooperation between testosterone and CXCR4 signaling involving astrocytes is required for myelin regeneration after focal demyelination produced in the
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Potential prognostic determinants for FET::CREB fusion-positive intracranial mesenchymal tumor Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-30 Frank M. Mezzacappa, Frankie K. Smith, Weiwei Zhang, Andrew Gard, Fatmagul Kusku Cabuk, Ignancio Gonzalez-Gomez, Hector L. Monforte, Jiancong Liang, Omkar Singh, Martha M. Quezado, Kenneth D. Aldape, Murat Gokden, Julia A. Bridge, Jie Chen
Intracranial mesenchymal tumor (IMT), FET::CREB fusion-positive is a provisional tumor type in the 2021 WHO classification of central nervous system tumors with limited information available. Herein, we describe five new IMT cases from four females and one male with three harboring an EWSR1::CREM fusion and two featuring an EWSR1::ATF1 fusion. Uniform manifold approximation and projection of DNA methylation
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Progesterone receptor distribution in the human hypothalamus and its association with suicide Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-23 Lin Zhang, Ronald W.H. Verwer, Joop van Heerikhuize, Paul J. Lucassen, Peter W. Nathanielsz, Elly M. Hol, Eleonora Aronica, Waljit S. Dhillo, Gerben Meynen, Dick F. Swaab
The human hypothalamus modulates mental health by balancing interactions between hormonal fluctuations and stress responses. Stress-induced progesterone release activates progesterone receptors (PR) in the human brain and triggers alterations in neuropeptides/neurotransmitters. As recent epidemiological studies have associated peripheral progesterone levels with suicide risks in humans, we mapped PR
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A rare non-gadolinium enhancing sarcoma brain metastasis with microenvironment dominated by tumor-associated macrophages Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-22 David Rogawski, Joshua Wheeler, Esther Nie, William Zhu, Eleanor Villanueva, Gwen Coffey, Qian Ma, Kristen Ganjoo, Nancy Fischbein, Michael Iv, Hannes Vogel, Seema Nagpal
Brain metastases occur in 1% of sarcoma cases and are associated with a median overall survival of 6 months. We report a rare case of a brain metastasis with unique radiologic and histopathologic features in a patient with low grade fibromyxoid sarcoma (LGFMS) previously treated with immune checkpoint inhibitor (ICI) therapy. The lone metastasis progressed in the midbrain tegmentum over 15 months as
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Missense mutation of NRAS is associated with malignant progression in neurocutaneous melanosis Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-22 Haruhiko Takahashi, Manabu Natsumeda, Norikazu Hara, Akihide Koyama, Hiroshi Shimizu, Akinori Miyashita, Daiken Satake, Yoshihiro Mouri, Jun Tsukano, Keita Kawabe, Yoshihiro Tsukamoto, Masayasu Okada, Ryosuke Ogura, Akihiko Yuki, Hajime Umezu, Akiyoshi Kakita, Takeshi Ikeuchi, Makoto Oishi
Neurocutaneous melanosis (NCM) is a rare congenital neurocutaneous syndrome characterized by congenital melanocytic nevus of skin and abnormal proliferation of leptomeningeal melanocytes. Early acquisition of post-zygotic somatic mutations has been postulated to underlie the pathogenesis of NCM. The pathogenesis of NCM remains to be fully elucidated, and treatment options have not been established
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The genomic alterations in glioblastoma influence the levels of CSF metabolites Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-19 Daniel H. Wang, Yoko Fujita, Antonio Dono, Ana G. Rodriguez Armendariz, Mauli Shah, Nagireddy Putluri, Pavel S. Pichardo-Rojas, Chirag B. Patel, Jay-Jiguang Zhu, Jason T. Huse, Brittany C. Parker Kerrigan, Frederick F. Lang, Yoshua Esquenazi, Leomar Y. Ballester
Cerebrospinal fluid (CSF) analysis is underutilized in patients with glioblastoma (GBM), partly due to a lack of studies demonstrating the clinical utility of CSF biomarkers. While some studies show the utility of CSF cell-free DNA analysis, studies analyzing CSF metabolites in patients with glioblastoma are limited. Diffuse gliomas have altered cellular metabolism. For example, mutations in isocitrate
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CNS erythroblastic sarcoma: a potential emerging pediatric tumor type characterized by NFIA::RUNX1T1/3 fusions Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-19 Arnault Tauziède-Espariat, Lucille Lew-Derivry, Samuel Abbou, Alice Métais, Gaëlle Pierron, Stéphanie Reynaud, Julien Masliah-Planchon, Cassandra Mariet, Lauren Hasty, Volodia Dangouloff-Ros, Nathalie Boddaert, Marie Csanyi, Aude Aline-Fardin, Claire Lamaison, Fabrice Chrétien, Kévin Beccaria, Stéphanie Puget, Pascale Varlet
Erythroblastic sarcoma (ES) (previously called chloroma or granulocytic sarcoma) are rare hematological neoplams characterized by the proliferation of myeloid blasts at extramedullary sites, and primarily involve the skin and soft tissue of middle-aged adults. ES may be concomitant with or secondary to myeloid neoplasms (mostly acute myeloid leukemia (AML)) or in isolated cases (de novo) without infiltration
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IFNγ drives neuroinflammation, demyelination, and neurodegeneration in a mouse model of multiple system atrophy Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-18 Nicole J. Corbin-Stein, Gabrielle M. Childers, Jhodi M. Webster, Asta Zane, Ya-Ting Yang, Nikhita Mudium, Rajesh Gupta, Fredric P. Manfredsson, Jeffrey H. Kordower, Ashley S. Harms
Multiple system atrophy (MSA) is a rare and fatal synucleinopathy characterized by insoluble alpha-synuclein (α-syn) cytoplasmic inclusions located within oligodendroglia. Neuroinflammation, demyelination, and neurodegeneration are correlated with areas of glia cytoplasmic inclusions (GCI) pathology, however it is not known what specifically drives disease pathogenesis. Recent studies have shown that
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MANF protein expression is upregulated in immune cells in the ischemic human brain and systemic recombinant MANF delivery in rat ischemic stroke model demonstrates anti-inflammatory effects Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-16 Jenni E. Anttila, Olli S. Mattila, Hock-Kean Liew, Kert Mätlik, Eero Mervaala, Päivi Lindholm, Maria Lindahl, Perttu J. Lindsberg, Kuan-Yin Tseng, Mikko Airavaara
Mesencephalic astrocyte-derived neurotrophic factor (MANF) has cytoprotective effects on various injuries, including cerebral ischemia, and it can promote recovery even when delivered intracranially several days after ischemic stroke. In the uninjured rodent brain, MANF protein is expressed almost exclusively in neurons, but post-ischemic MANF expression has not been characterized. We aimed to investigate
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Unclassifiable CNS tumors in DNA methylation-based classification: clinical challenges and prognostic impact Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-16 Richard Drexler, Florian Brembach, Jennifer Sauvigny, Franz L. Ricklefs, Alicia Eckhardt, Helena Bode, Jens Gempt, Katrin Lamszus, Manfred Westphal, Ulrich Schüller, Malte Mohme
DNA methylation analysis has become a powerful tool in neuropathology. Although DNA methylation-based classification usually shows high accuracy, certain samples cannot be classified and remain clinically challenging. We aimed to gain insight into these cases from a clinical perspective. To address, central nervous system (CNS) tumors were subjected to DNA methylation profiling and classified according
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CNS tumor with CREBBP::BCORL1 Fusion and pathogenic mutations in BCOR and CREBBP: expanding the spectrum of BCOR-altered tumors Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-12 Valeria Barresi, Antonello Cardoni, Evelina Miele, Lucia Pedace, Barbara Masotto, Claudia Nardini, Sabina Barresi, Sabrina Rossi
The fifth edition of the World Health Organization (WHO) classification of central nervous system (CNS) tumors introduced the new tumor type CNS tumor with BCOR internal tandem duplication (ITD), characterized by a distinct DNA methylation profile and peculiar histopathological features, including a circumscribed growth pattern, ependymoma-like perivascular pseudorosettes, microcystic pattern, absent
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Enhancing mitosis quantification and detection in meningiomas with computational digital pathology Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-11 Hongyan Gu, Chunxu Yang, Issa Al-kharouf, Shino Magaki, Nelli Lakis, Christopher Kazu Williams, Sallam Mohammad Alrosan, Ellie Kate Onstott, Wenzhong Yan, Negar Khanlou, Inma Cobos, Xinhai Robert Zhang, Neda Zarrin-Khameh, Harry V. Vinters, Xiang Anthony Chen, Mohammad Haeri
Mitosis is a critical criterion for meningioma grading. However, pathologists’ assessment of mitoses is subject to significant inter-observer variation due to challenges in locating mitosis hotspots and accurately detecting mitotic figures. To address this issue, we leverage digital pathology and propose a computational strategy to enhance pathologists’ mitosis assessment. The strategy has two components:
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Cerebrospinal fluid shotgun proteomics identifies distinct proteomic patterns in cerebral amyloid angiopathy rodent models and human patients Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-08 Marc Vervuurt, Joseph M. Schrader, Anna M. de Kort, Iris Kersten, Hans J. C. T. Wessels, Catharina J. M. Klijn, Floris H. B. M. Schreuder, H. Bea Kuiperij, Jolein Gloerich, William E. Van Nostrand, Marcel M. Verbeek
Cerebral amyloid angiopathy (CAA) is a form of small vessel disease characterised by the progressive deposition of amyloid β protein in the cerebral vasculature, inducing symptoms including cognitive impairment and cerebral haemorrhages. Due to their accessibility and homogeneous disease phenotypes, animal models are advantageous platforms to study diseases like CAA. Untargeted proteomics studies of
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Bi-directional regulation of AIMP2 and its splice variant on PARP-1-dependent neuronal cell death; Therapeutic implication for Parkinson's disease Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-03 Min Hak Lee, Ki-Hwan Um, Seok Won Lee, Ye Ji Sun, Da-Hye Gu, Young Ok Jo, Sung Hyun Kim, Wongi Seol, Hyorin Hwang, Kyunghwa Baek, Jin Woo Choi
Parthanatos represents a critical molecular aspect of Parkinson's disease, wherein AIMP2 aberrantly activates PARP-1 through direct physical interaction. Although AIMP2 ought to be a therapeutic target for the disease, regrettably, it is deemed undruggable due to its non-enzymatic nature and predominant localization within the tRNA synthetase multi-complex. Instead, AIMP2 possesses an antagonistic
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Regional differences in synaptic degeneration are linked to alpha-synuclein burden and axonal damage in Parkinson’s disease and dementia with Lewy bodies Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-03 Irene Frigerio, Maud M. A. Bouwman, Ruby T. G. M. M. Noordermeer, Ema Podobnik, Marko Popovic, Evelien Timmermans, Annemieke J. M. Rozemuller, Wilma D. J. van de Berg, Laura E. Jonkman
Regional differences in synaptic degeneration may underlie differences in clinical presentation and neuropathological disease progression in Parkinson’s Disease (PD) and Dementia with Lewy bodies (DLB). Here, we mapped and quantified synaptic degeneration in cortical brain regions in PD, PD with dementia (PDD) and DLB, and assessed whether regional differences in synaptic loss are linked to axonal
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Histone acetylation in an Alzheimer’s disease cell model promotes homeostatic amyloid-reducing pathways Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-02 Daniel C. Xu, Hanna Sas-Nowosielska, Greg Donahue, Hua Huang, Naemeh Pourshafie, Charly R. Good, Shelley L. Berger
Alzheimer’s Disease (AD) is a disorder characterized by cognitive decline, neurodegeneration, and accumulation of amyloid plaques and tau neurofibrillary tangles in the brain. Dysregulation of epigenetic histone modifications may lead to expression of transcriptional programs that play a role either in protecting against disease genesis or in worsening of disease pathology. One such histone modification
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Letter to the editor on: Hornerin deposits in neuronal intranuclear inclusion disease: direct identification of proteins with compositionally biased regions in inclusions by Park et al. (2022) Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-02 Huihui Luo, Emil K. Gustavsson, Hannah Macpherson, Natalia Dominik, Kristina Zhelcheska, Kylie Montgomery, Claire Anderson, Wai Yan Yau, Stephanie Efthymiou, Chris Turner, Michael DeTure, Dennis W. Dickson, Keith A. Josephs, Tamas Revesz, Tammaryn Lashley, Glenda Halliday, Dominic B. Rowe, Emily McCann, Ian Blair, Andrew J. Lees, Pentti J. Tienari, Anu Suomalainen, Laura Molina-Porcel, Gabor G. Kovacs
We read with interest the work by Park and colleagues, which attempted to elucidate the composition of neuronal intranuclear inclusions (NIIs), central to the pathology of neuronal intranuclear inclusion disease (NIID) [1]. NIID is a clinically heterogeneous neurodegenerative disorder characterised by these intranuclear eosinophilic ubiquitinated inclusions in both neuronal and non-neuronal cells [2]
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Distinct forebrain regions define a dichotomous astrocytic profile in multiple system atrophy Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2024-01-02 Y. Schneider, C. Gauer, M. Andert, A. Hoffmann, M. J. Riemenschneider, W. Krebs, N. Chalmers, C. Lötzsch, U. J. Naumann, W. Xiang, V. Rothhammer, R. Beckervordersandforth, J. C. M. Schlachetzki, J. Winkler
The growing recognition of a dichotomous role of astrocytes in neurodegenerative processes has heightened the need for unraveling distinct astrocytic subtypes in neurological disorders. In multiple system atrophy (MSA), a rare, rapidly progressing atypical Parkinsonian disease characterized by increased astrocyte reactivity. However the specific contribution of astrocyte subtypes to neuropathology
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Unsupervised machine learning identifies distinct ALS molecular subtypes in post-mortem motor cortex and blood expression data Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-21 Heather Marriott, Renata Kabiljo, Guy P Hunt, Ahmad Al Khleifat, Ashley Jones, Claire Troakes, Abigail L Pfaff, John P Quinn, Sulev Koks, Richard J Dobson, Patrick Schwab, Ammar Al-Chalabi, Alfredo Iacoangeli
Amyotrophic lateral sclerosis (ALS) displays considerable clinical and genetic heterogeneity. Machine learning approaches have previously been utilised for patient stratification in ALS as they can disentangle complex disease landscapes. However, lack of independent validation in different populations and tissue samples have greatly limited their use in clinical and research settings. We overcame these
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Clinicopathologic features of two unrelated autopsied patients with Charcot-Marie-Tooth disease carrying MFN2 gene mutation Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-20 Hideki Hayashi, Rie Saito, Hidetomo Tanaka, Norikazu Hara, Shin Koide, Yosuke Yonemochi, Tetsuo Ozawa, Mariko Hokari, Yasuko Toyoshima, Akinori Miyashita, Osamu Onodera, Kouichirou Okamoto, Takeshi Ikeuchi, Takashi Nakajima, Akiyoshi Kakita
To the editor Charcot-Marie-Tooth disease type 2A2 (CMT2A2) is the second most common type of CMT, characterized by axonal neuropathy, and 9–20% of affected patients present with optic atrophy [6, 8]. It is caused by mutations in the mitofusin2 (MFN2), which encodes a component of the outer mitochondrial membrane, and is essential for mitochondrial fusion [2]. Although a number of clinical studies
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Genetic ablation of Sarm1 attenuates expression and mislocalization of phosphorylated TDP-43 after mouse repetitive traumatic brain injury Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-20 Elif O. Dogan, James Bouley, Jianjun Zhong, Ashley L. Harkins, Allison M. Keeler, Daryl A. Bosco, Robert H. Brown, Nils Henninger
Traumatic brain injury (TBI), particularly when moderate-to-severe and repetitive, is a strong environmental risk factor for several progressive neurodegenerative disorders. Mislocalization and deposition of transactive response DNA binding protein 43 (TDP-43) has been reported in both TBI and TBI-associated neurodegenerative diseases. It has been hypothesized that axonal pathology, an early event
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Association between APOE-ε4 allele and cognitive function is mediated by Alzheimer’s disease pathology: a population-based autopsy study in an admixed sample Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-19 Regina Silva Paradela, Alberto Fernando Oliveira Justo, Vítor Ribeiro Paes, Renata E. P. Leite, Carlos A. Pasqualucci, Lea T. Grinberg, Michel Satya Naslavsky, Mayana Zatz, Ricardo Nitrini, Wilson Jacob-Filho, Claudia Kimie Suemoto
Apolipoprotein E ε4 allele (APOE-ε4) is the main genetic risk factor for late-onset Alzheimer’s disease (AD) and may impact cognitive function also via other neuropathological lesions. However, there is limited evidence available from diverse populations, as APOE associations with dementia seem to differ by race. Therefore, we aimed to evaluate the pathways linking APOE-ε4 to cognitive abilities through
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Spatio-temporal dynamics of microglia phenotype in human and murine cSVD: impact of acute and chronic hypertensive states Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-19 Lorena Morton, Philipp Arndt, Alejandra P. Garza, Solveig Henneicke, Hendrik Mattern, Marilyn Gonzalez, Alexander Dityatev, Deniz Yilmazer-Hanke, Stefanie Schreiber, Ildiko R. Dunay
Vascular risk factors such as chronic hypertension are well-established major modifiable factors for the development of cerebral small vessel disease (cSVD). In the present study, our focus was the investigation of cSVD-related phenotypic changes in microglia in human disease and in the spontaneously hypertensive stroke-prone rat (SHRSP) model of cSVD. Our examination of cortical microglia in human
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miRNA-211 maintains metabolic homeostasis in medulloblastoma through its target gene long-chain acyl-CoA synthetase 4 Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-19 Menglang Yuan, Iqbal Mahmud, Keisuke Katsushima, Kandarp Joshi, Olivier Saulnier, Rudramani Pokhrel, Bongyong Lee, Wathsala Liyanage, Haritha Kunhiraman, Stacie Stapleton, Ignacio Gonzalez-Gomez, Rangaramanujam M. Kannan, Tanja Eisemann, Elayaraja Kolanthai, Sudipta Seal, Timothy J. Garrett, Saed Abbasi, Kimberly Bockley, Justin Hanes, Prem Chapagain, George Jallo, Robert J. Wechsler-Reya, Michael
The prognosis of childhood medulloblastoma (MB) is often poor, and it usually requires aggressive therapy that adversely affects quality of life. microRNA-211 (miR-211) was previously identified as an important regulator of cells that descend from neural cells. Since medulloblastomas primarily affect cells with similar ontogeny, we investigated the role and mechanism of miR-211 in MB. Here we showed
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Toward a generalizable machine learning workflow for neurodegenerative disease staging with focus on neurofibrillary tangles Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-18 Juan C. Vizcarra, Thomas M. Pearce, Brittany N. Dugger, Michael J. Keiser, Marla Gearing, John F. Crary, Evan J. Kiely, Meaghan Morris, Bartholomew White, Jonathan D. Glass, Kurt Farrell, David A. Gutman
Machine learning (ML) has increasingly been used to assist and expand current practices in neuropathology. However, generating large imaging datasets with quality labels is challenging in fields which demand high levels of expertise. Further complicating matters is the often seen disagreement between experts in neuropathology-related tasks, both at the case level and at a more granular level. Neurofibrillary
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Cellular and subcellular localization of Rab10 and phospho-T73 Rab10 in the mouse and human brain Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-18 Vijay Singh, Marissa A. Menard, Geidy E. Serrano, Thomas G. Beach, Hien T. Zhao, Alexis Riley-DiPaolo, Nitya Subrahmanian, Matthew J. LaVoie, Laura A. Volpicelli-Daley
Autosomal dominant pathogenic mutations in Leucine-rich repeat kinase 2 (LRRK2) cause Parkinson’s disease (PD). The most common mutation, G2019S-LRRK2, increases the kinase activity of LRRK2 causing hyper-phosphorylation of its substrates. One of these substrates, Rab10, is phosphorylated at a conserved Thr73 residue (pRab10), and is one of the most abundant LRRK2 Rab GTPases expressed in various tissues
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Targeting RACK1 to alleviate TDP-43 and FUS proteinopathy-mediated suppression of protein translation and neurodegeneration Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-18 Beibei Zhao, Catherine M. Cowan, Juliane A. Coutts, Darren D. Christy, Ananya Saraph, Shawn C. C. Hsueh, Stephen S. Plotkin, Ian R. Mackenzie, Johanne M. Kaplan, Neil R. Cashman
TAR DNA-binding protein 43 (TDP-43) and Fused in Sarcoma/Translocated in Sarcoma (FUS) are ribonucleoproteins associated with pathogenesis of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Under physiological conditions, TDP-43 and FUS are predominantly localized in the nucleus, where they participate in transcriptional regulation, RNA splicing and metabolism. In
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Mimicking hypomethylation of FUS requires liquid–liquid phase separation to induce synaptic dysfunctions Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-18 Seung Chan Kim, Scott J. Mitchell, Seema Qamar, Daniel J. Whitcomb, Marc-David Ruepp, Peter St George-Hyslop, Kwangwook Cho
The hypomethylation of fused in sarcoma (FUS) in frontotemporal lobar degeneration promotes the formation of irreversible condensates of FUS. However, the mechanisms by which these hypomethylated FUS condensates cause neuronal dysfunction are unknown. Here we report that expression of FUS constructs mimicking hypomethylated FUS causes aberrant dendritic FUS condensates in CA1 neurons. These hypomethylated
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A novel patient-derived meningioma spheroid model as a tool to study and treat epithelial-to-mesenchymal transition (EMT) in meningiomas Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-15 Laurien L. van de Weijer, Emanuela Ercolano, Ting Zhang, Maryam Shah, Matthew C. Banton, Juri Na, Claire L. Adams, David Hilton, Kathreena M. Kurian, C. Oliver Hanemann
Meningiomas are the most common intracranial brain tumours. These tumours are heterogeneous and encompass a wide spectrum of clinical aggressivity. Treatment options are limited to surgery and radiotherapy and have a risk of post-operative morbidities and radiation neurotoxicity, reflecting the need for new therapies. Three-dimensional (3D) patient-derived cell culture models have been shown to closely
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ApoER2-Dab1 disruption as the origin of pTau-associated neurodegeneration in sporadic Alzheimer’s disease Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-13 Christopher E. Ramsden, Daisy Zamora, Mark S. Horowitz, Jahandar Jahanipour, Elizabeth Calzada, Xiufeng Li, Gregory S. Keyes, Helen C. Murray, Maurice A. Curtis, Richard M. Faull, Andrea Sedlock, Dragan Maric
In sporadic Alzheimer’s disease (sAD) specific regions, layers and neurons accumulate hyperphosphorylated Tau (pTau) and degenerate early while others remain unaffected even in advanced disease. ApoER2-Dab1 signaling suppresses Tau phosphorylation as part of a four-arm pathway that regulates lipoprotein internalization and the integrity of actin, microtubules, and synapses; however, the role of this
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Nuclear face of Tau: an inside player in neurodegeneration Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-12 Neelam Younas, Tayyaba Saleem, Abrar Younas, Inga Zerr
Tau (Tubulin associated unit) protein is a major hallmark of Alzheimer’s disease (AD) and tauopathies. Tau is predominantly an axonal protein with a crucial role in the stabilization and dynamics of the microtubules. Since the discovery of Tau protein in 1975, research efforts were concentrated on the pathophysiological role of Tau protein in the context of the microtubules. Although, for more than
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Cortical microvascular raspberries and ageing: an independent but not exclusive relationship Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-12 Henric Ek Olofsson, Thea Österling Delshammar, Elisabet Englund
Raspberries are cerebral microvascular formations of unknown origin, defined as three or more transversally sectioned vascular lumina surrounded by a common perivascular space. We have previously demonstrated an increased raspberry density in the cortex of patients with vascular dementia and cerebral atherosclerosis, while studies by other authors on overlapping and synonymously defined vascular entities
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A novel BRAF::PTPRN2 fusion in meningioma: a case report Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-08 Nishanth S. Sadagopan, Khizar R. Nandoliya, Mark W. Youngblood, Craig M. Horbinski, Jared T. Ahrendsen, Stephen T. Magill
Gene fusion events have been linked to oncogenesis in many cancers. However, gene fusions in meningioma are understudied compared to somatic mutations, chromosomal gains/losses, and epigenetic changes. Fusions involving B-raf proto-oncogene, serine/threonine kinase (BRAF) are subtypes of oncogenic BRAF genetic abnormalities that have been reported in certain cases of brain tumors, such as pilocytic
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Post-COVID exercise intolerance is associated with capillary alterations and immune dysregulations in skeletal muscles Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-08 Tom Aschman, Emanuel Wyler, Oliver Baum, Andreas Hentschel, Rebekka Rust, Franziska Legler, Corinna Preusse, Lil Meyer-Arndt, Ivana Büttnerova, Alexandra Förster, Derya Cengiz, Luiz Gustavo Teixeira Alves, Julia Schneider, Claudia Kedor, Judith Bellmann-Strobl, Aminaa Sanchin, Hans-Hilmar Goebel, Markus Landthaler, Victor Corman, Andreas Roos, Frank L. Heppner, Helena Radbruch, Friedemann Paul, Carmen
The SARS-CoV-2 pandemic not only resulted in millions of acute infections worldwide, but also in many cases of post-infectious syndromes, colloquially referred to as “long COVID”. Due to the heterogeneous nature of symptoms and scarcity of available tissue samples, little is known about the underlying mechanisms. We present an in-depth analysis of skeletal muscle biopsies obtained from eleven patients
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Glioblastoma pseudoprogression and true progression reveal spatially variable transcriptional differences Acta Neuropathol. Commun. (IF 7.1) Pub Date : 2023-12-04 Wesley Wang, Jonah Domingo Tugaoen, Paolo Fadda, Amanda Ewart Toland, Qin Ma, J. Brad Elder, Pierre Giglio, José Javier Otero
Post-resection radiologic monitoring to identify areas of new or progressive enhancement concerning for cancer recurrence is critical during patients with glioblastoma follow-up. However, treatment-related pseudoprogression presents with similar imaging features but requires different clinical management. While pathologic diagnosis is the gold standard to differentiate true progression and pseudoprogression