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Your search keyword '"Herms, Jochen"' showing total 11 results
Start Over Author "Herms, Jochen" Journal acta neuropathologica communications
11 results on '"Herms, Jochen"'

1. Translocator protein (18kDA) (TSPO) marks mesenchymal glioblastoma cell populations characterized by elevated numbers of tumor-associated macrophages

Author

Weidner, Lorraine, Lorenz, Julia, Quach, Stefanie, Braun, Frank K., Rothhammer-Hampl, Tanja, Ammer, Laura-Marie, Vollmann-Zwerenz, Arabel, Bartos, Laura M., Dekorsy, Franziska J., Holzgreve, Adrien, Kirchleitner, Sabrina V., Thon, Niklas, Greve, Tobias, Ruf, Viktoria, Herms, Jochen, Bader, Stefanie, Milenkovic, Vladimir M., von Baumgarten, Louisa, Menevse, Ayse N., Hussein, Abir, Sax, Julian, Wetzel, Christian H., Rupprecht, Rainer, Proescholdt, Martin, Schmidt, Nils O., Beckhove, Philipp, Hau, Peter, Tonn, Joerg-Christian, Bartenstein, Peter, Brendel, Matthias, Albert, Nathalie L., and Riemenschneider, Markus J.

Published
2023
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2. Targeting the glycine-rich domain of TDP-43 with antibodies prevents its aggregation in vitro and reduces neurofilament levels in vivo

Author

Riemenschneider, Henrick, Simonetti, Francesca, Sheth, Udit, Katona, Eszter, Roth, Stefan, Hutten, Saskia, Farny, Daniel, Michaelsen, Meike, Nuscher, Brigitte, Schmidt, Michael K., Flatley, Andrew, Schepers, Aloys, Gruijs da Silva, Lara A., Zhou, Qihui, Klopstock, Thomas, Liesz, Arthur, Arzberger, Thomas, Herms, Jochen, Feederle, Regina, Gendron, Tania F., Dormann, Dorothee, and Edbauer, Dieter

Published
2023
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4. TP53 mutations in functional corticotroph tumors are linked to invasion and worse clinical outcome

Author

Perez-Rivas, Luis Gustavo, Simon, Julia, Albani, Adriana, Tang, Sicheng, Roeber, Sigrun, Assié, Guillaume, Deutschbein, Timo, Fassnacht, Martin, Gadelha, Monica R., Hermus, Ad R., Stalla, Günter K., Tichomirowa, Maria A., Rotermund, Roman, Flitsch, Jörg, Buchfelder, Michael, Nasi-Kordhishti, Isabella, Honegger, Jürgen, Thorsteinsdottir, Jun, Saeger, Wolfgang, Herms, Jochen, Reincke, Martin, and Theodoropoulou, Marily

Published
2022
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11. High plasticity of axonal pathology in Alzheimer’s disease mouse models

Author

Blazquez-Llorca, Lidia, Valero-Freitag, Susana, Rodrigues, Eva Ferreira, Merchán-Pérez, Ángel, Rodríguez, J. Rodrigo, Dorostkar, Mario M., DeFelipe, Javier, Herms, Jochen, Ministerio de Economía y Competitividad (España), Centro Investigación Biomédica en Red Enfermedades Neurodegenerativas (España), Alzheimer's Association, and Alexander von Humboldt Foundation

Subjects
Green Fluorescent Proteins, Plaque, Amyloid, Mice, Transgenic, metabolism [Axons], Dystrophic neurites, APP protein, human, pathology [Alzheimer Disease], Amyloid beta-Protein Precursor, PSEN1 protein, human, Imaging, Three-Dimensional, Microscopy, Electron, Transmission, Alzheimer Disease, metabolism [Amyloid beta-Protein Precursor], Presenilin-1, Animals, genetics [Green Fluorescent Proteins], Humans, ddc:610, pathology [Plaque, Amyloid], Two-photon microscopy, Cell Size, Neuronal Plasticity, pathology [Axons], metabolism [Presenilin-1], Research, Somatosensory Cortex, genetics [Presenilin-1], pathology [Somatosensory Cortex], FIB/SEM microscopy, Axons, metabolism [Plaque, Amyloid], Disease Models, Animal, Microscopy, Fluorescence, nervous system, genetics [Amyloid beta-Protein Precursor], metabolism [Green Fluorescent Proteins], Microscopy, Electron, Scanning, metabolism [Somatosensory Cortex], Three-dimensional, Alzheimer’s disease, metabolism [Alzheimer Disease]
Abstract

© The Author(s)., Axonal dystrophies (AxDs) are swollen and tortuous neuronal processes that are associated with extracellular depositions of amyloid β (Aβ) and have been observed to contribute to synaptic alterations occurring in Alzheimer’s disease. Understanding the temporal course of this axonal pathology is of high relevance to comprehend the progression of the disease over time. We performed a long-term in vivo study (up to 210 days of two-photon imaging) with two transgenic mouse models (dE9xGFP-M and APP-PS1xGFP-M). Interestingly, AxDs were formed only in a quarter of GFP-expressing axons near Aβ-plaques, which indicates a selective vulnerability. AxDs, especially those reaching larger sizes, had long lifetimes and appeared as highly plastic structures with large variations in size and shape and axonal sprouting over time. In the case of the APP-PS1 mouse only, the formation of new long axonal segments in dystrophic axons (re-growth phenomenon) was observed. Moreover, new AxDs could appear at the same point of the axon where a previous AxD had been located before disappearance (re-formation phenomenon). In addition, we observed that most AxDs were formed and developed during the imaging period, and numerous AxDs had already disappeared by the end of this time. This work is the first in vivo study analyzing quantitatively the high plasticity of the axonal pathology around Aβ plaques. We hypothesized that a therapeutically early prevention of Aβ plaque formation or their growth might halt disease progression and promote functional axon regeneration and the recovery of neural circuits., The work was supported by grants from the Spanish Ministry of Economy and Competitiveness (MINECO) (BFU2012-34963 to JF), the Centre for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED, CB06/05/0066) (to JF), a grant from the Alzheimer’s Association (ZEN-15-321663) (to JF) and the Humboldt Research Fellowship for Postdoctoral Researchers (LBL).

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