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493 results on '"Herms, Jochen"'

1. Plasma extracellular vesicle tau and TDP-43 as diagnostic biomarkers in FTD and ALS

Author

Chatterjee, Madhurima, Özdemir, Selcuk, Fritz, Christian, Möbius, Wiebke, Kleineidam, Luca, Mandelkow, Eckhard, Biernat, Jacek, Doğdu, Cem, Peters, Oliver, Cosma, Nicoleta Carmen, Wang, Xiao, Schneider, Luisa-Sophia, Priller, Josef, Spruth, Eike, Kühn, Andrea A., Krause, Patricia, Klockgether, Thomas, Vogt, Ina R., Kimmich, Okka, Spottke, Annika, Hoffmann, Daniel C., Fliessbach, Klaus, Miklitz, Carolin, McCormick, Cornelia, Weydt, Patrick, Falkenburger, Björn, Brandt, Moritz, Guenther, René, Dinter, Elisabeth, Wiltfang, Jens, Hansen, Niels, Bähr, Mathias, Zerr, Inga, Flöel, Agnes, Nestor, Peter J., Düzel, Emrah, Glanz, Wenzel, Incesoy, Enise, Bürger, Katharina, Janowitz, Daniel, Perneczky, Robert, Rauchmann, Boris S., Hopfner, Franziska, Wagemann, Olivia, Levin, Johannes, Teipel, Stefan, Kilimann, Ingo, Goerss, Doreen, Prudlo, Johannes, Gasser, Thomas, Brockmann, Kathrin, Mengel, David, Zimmermann, Milan, Synofzik, Matthis, Wilke, Carlo, Selma-González, Judit, Turon-Sans, Janina, Santos-Santos, Miguel Angel, Alcolea, Daniel, Rubio-Guerra, Sara, Fortea, Juan, Carbayo, Álvaro, Lleó, Alberto, Rojas-García, Ricardo, Illán-Gala, Ignacio, Wagner, Michael, Frommann, Ingo, Roeske, Sandra, Bertram, Lucas, Heneka, Michael T., Brosseron, Frederic, Ramirez, Alfredo, Schmid, Matthias, Beschorner, Rudi, Halle, Annett, Herms, Jochen, Neumann, Manuela, Barthélemy, Nicolas R., Bateman, Randall J., Rizzu, Patrizia, Heutink, Peter, Dols-Icardo, Oriol, Höglinger, Günter, Hermann, Andreas, and Schneider, Anja

Published
2024
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2. Regional desynchronization of microglial activity is associated with cognitive decline in Alzheimer’s disease

Author

Zatcepin, Artem, Gnörich, Johannes, Rauchmann, Boris-Stephan, Bartos, Laura M., Wagner, Stephan, Franzmeier, Nicolai, Malpetti, Maura, Xiang, Xianyuan, Shi, Yuan, Parhizkar, Samira, Grosch, Maximilian, Wind-Mark, Karin, Kunte, Sebastian T., Beyer, Leonie, Meyer, Carolin, Brösamle, Desirée, Wendeln, Ann-Christin, Osei-Sarpong, Collins, Heindl, Steffanie, Liesz, Arthur, Stoecklein, Sophia, Biechele, Gloria, Finze, Anika, Eckenweber, Florian, Lindner, Simon, Rominger, Axel, Bartenstein, Peter, Willem, Michael, Tahirovic, Sabina, Herms, Jochen, Buerger, Katharina, Simons, Mikael, Haass, Christian, Rupprecht, Rainer, Riemenschneider, Markus J., Albert, Nathalie L., Beyer, Marc, Neher, Jonas J., Paeger, Lars, Levin, Johannes, Höglinger, Günter U., Perneczky, Robert, Ziegler, Sibylle I., and Brendel, Matthias

Published
2024
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4. Common Variants Near ZIC1 and ZIC4 in Autopsy-Confirmed Multiple System Atrophy.

Author

Hopfner, Franziska, Tietz, Anja, Ruf, Viktoria, Ross, Owen, Koga, Shunsuke, Dickson, Dennis, Aguzzi, Adriano, Attems, Johannes, Beach, Thomas, Beller, Allison, Cheshire, William, van Deerlin, Vivianna, Deuschl, Günther, Duyckaerts, Charles, Ellinghaus, David, Evsyukov, Valentin, Flanagan, Margaret, Franke, Andre, Frosch, Matthew, Gearing, Marla, Gelpi, Ellen, van Gerpen, Jay, Ghetti, Bernardino, Glass, Jonathan, Halliday, Glenda, Helbig, Ingo, Höllerhage, Matthias, Huitinga, Inge, Irwin, David, Keene, Dirk, Kovacs, Gabor, Lee, Edward, Levin, Johannes, Martí, Maria, Mackenzie, Ian, McKeith, Ian, Mclean, Catriona, Mollenhauer, Brit, Neumann, Manuela, Newell, Kathy, Pantelyat, Alex, Pendziwiat, Manuela, Peters, Annette, Molina Porcel, Laura, Rabano, Alberto, Matěj, Radoslav, Rajput, Alex, Rajput, Ali, Reimann, Regina, Scott, William, Selvackadunco, Sashika, Simuni, Tanya, Stadelmann, Christine, Svenningsson, Per, Thomas, Alan, Trenkwalder, Claudia, Troakes, Claire, Trojanowski, John, Uitti, Ryan, White, Charles, Wszolek, Zbigniew, Xie, Tao, Ximelis, Teresa, Yebenes, Justo, Müller, Ulrich, Schellenberg, Gerard, Herms, Jochen, Kuhlenbäumer, Gregor, Höglinger, Günter, Grinberg, Lea, Seeley, William, and Desplats, Paula

Subjects
ZIC1, ZIC4, autopsy-confirmed, genome-wide association study, multiple system atrophy, Autoantibodies, Autopsy, Genome-Wide Association Study, Humans, Multiple System Atrophy, Nerve Tissue Proteins, Olivopontocerebellar Atrophies, Striatonigral Degeneration, Transcription Factors, alpha-Synuclein
Abstract

BACKGROUND: Multiple System Atrophy is a rare neurodegenerative disease with alpha-synuclein aggregation in glial cytoplasmic inclusions and either predominant olivopontocerebellar atrophy or striatonigral degeneration, leading to dysautonomia, parkinsonism, and cerebellar ataxia. One prior genome-wide association study in mainly clinically diagnosed patients with Multiple System Atrophy failed to identify genetic variants predisposing for the disease. OBJECTIVE: Since the clinical diagnosis of Multiple System Atrophy yields a high rate of misdiagnosis when compared to the neuropathological gold standard, we studied only autopsy-confirmed cases. METHODS: We studied common genetic variations in Multiple System Atrophy cases (N = 731) and controls (N = 2898). RESULTS: The most strongly disease-associated markers were rs16859966 on chromosome 3, rs7013955 on chromosome 8, and rs116607983 on chromosome 4 with P-values below 5 × 10-6 , all of which were supported by at least one additional genotyped and several imputed single nucleotide polymorphisms. The genes closest to the chromosome 3 locus are ZIC1 and ZIC4 encoding the zinc finger proteins of cerebellum 1 and 4 (ZIC1 and ZIC4). INTERPRETATION: Since mutations of ZIC1 and ZIC4 and paraneoplastic autoantibodies directed against ZIC4 are associated with severe cerebellar dysfunction, we conducted immunohistochemical analyses in brain tissue of the frontal cortex and the cerebellum from 24 Multiple System Atrophy patients. Strong immunohistochemical expression of ZIC4 was detected in a subset of neurons of the dentate nucleus in all healthy controls and in patients with striatonigral degeneration, whereas ZIC4-immunoreactive neurons were significantly reduced inpatients with olivopontocerebellar atrophy. These findings point to a potential ZIC4-mediated vulnerability of neurons in Multiple System Atrophy. © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Published
2022

5. Towards multicenter β-amyloid PET imaging in mouse models: A triple scanner head-to-head comparison

Author

Gnörich, Johannes, Koehler, Mara, Wind-Mark, Karin, Klaus, Carolin, Zatcepin, Artem, Palumbo, Giovanna, Lalia, Manvir, Monasor, Laura Sebastian, Beyer, Leonie, Eckenweber, Florian, Scheifele, Maximilian, Gildehaus, Franz-Josef, von Ungern-Sternberg, Barbara, Barthel, Henryk, Sabri, Osama, Bartenstein, Peter, Herms, Jochen, Tahirovic, Sabina, Franzmeier, Nicolai, Ziegler, Sibylle, and Brendel, Matthias

Published
2024
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6. 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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7. 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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8. Depletion and activation of microglia impact metabolic connectivity of the mouse brain

Author

Gnörich, Johannes, Reifschneider, Anika, Wind, Karin, Zatcepin, Artem, Kunte, Sebastian T., Beumers, Philipp, Bartos, Laura M., Wiedemann, Thomas, Grosch, Maximilian, Xiang, Xianyuan, Fard, Maryam K., Ruch, Francois, Werner, Georg, Koehler, Mara, Slemann, Luna, Hummel, Selina, Briel, Nils, Blume, Tanja, Shi, Yuan, Biechele, Gloria, Beyer, Leonie, Eckenweber, Florian, Scheifele, Maximilian, Bartenstein, Peter, Albert, Nathalie L., Herms, Jochen, Tahirovic, Sabina, Haass, Christian, Capell, Anja, Ziegler, Sibylle, and Brendel, Matthias

Published
2023
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10. [18F]F-DED PET imaging of reactive astrogliosis in neurodegenerative diseases: preclinical proof of concept and first-in-human data

Author

Ballweg, Anna, Klaus, Carolin, Vogler, Letizia, Katzdobler, Sabrina, Wind, Karin, Zatcepin, Artem, Ziegler, Sibylle I., Secgin, Birkan, Eckenweber, Florian, Bohr, Bernd, Bernhardt, Alexander, Fietzek, Urban, Rauchmann, Boris-Stephan, Stoecklein, Sophia, Quach, Stefanie, Beyer, Leonie, Scheifele, Maximilian, Simmet, Marcel, Joseph, Emanuel, Lindner, Simon, Berg, Isabella, Koglin, Norman, Mueller, Andre, Stephens, Andrew W., Bartenstein, Peter, Tonn, Joerg C., Albert, Nathalie L., Kümpfel, Tania, Kerschensteiner, Martin, Perneczky, Robert, Levin, Johannes, Paeger, Lars, Herms, Jochen, and Brendel, Matthias

Published
2023
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12. Tau deposition patterns are associated with functional connectivity in primary tauopathies

Author

Franzmeier, Nicolai, Brendel, Matthias, Beyer, Leonie, Slemann, Luna, Kovacs, Gabor G, Arzberger, Thomas, Kurz, Carolin, Respondek, Gesine, Lukic, Milica J, Biel, Davina, Rubinski, Anna, Frontzkowski, Lukas, Hummel, Selina, Müller, Andre, Finze, Anika, Palleis, Carla, Joseph, Emanuel, Weidinger, Endy, Katzdobler, Sabrina, Song, Mengmeng, Biechele, Gloria, Kern, Maike, Scheifele, Maximilian, Rauchmann, Boris-Stephan, Perneczky, Robert, Rullman, Michael, Patt, Marianne, Schildan, Andreas, Barthel, Henryk, Sabri, Osama, Rumpf, Jost J, Schroeter, Matthias L, Classen, Joseph, Villemagne, Victor, Seibyl, John, Stephens, Andrew W, Lee, Edward B, Coughlin, David G, Giese, Armin, Grossman, Murray, McMillan, Corey T, Gelpi, Ellen, Molina-Porcel, Laura, Compta, Yaroslau, van Swieten, John C, Laat, Laura Donker, Troakes, Claire, Al-Sarraj, Safa, Robinson, John L, Xie, Sharon X, Irwin, David J, Roeber, Sigrun, Herms, Jochen, Simons, Mikael, Bartenstein, Peter, Lee, Virginia M, Trojanowski, John Q, Levin, Johannes, Höglinger, Günter, and Ewers, Michael

Subjects
Biochemistry and Cell Biology, Biological Sciences, Acquired Cognitive Impairment, Rare Diseases, Brain Disorders, Pick's Disease, Alzheimer's Disease, Dementia, Frontotemporal Dementia (FTD), Neurosciences, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Neurodegenerative, Aging, Alzheimer's Disease Related Dementias (ADRD), Biomedical Imaging, Aetiology, 2.1 Biological and endogenous factors, Neurological, Brain, Humans, Magnetic Resonance Imaging, Supranuclear Palsy, Progressive, Tauopathies, tau Proteins
Abstract

Tau pathology is the main driver of neuronal dysfunction in 4-repeat tauopathies, including cortico-basal degeneration and progressive supranuclear palsy. Tau is assumed to spread prion-like across connected neurons, but the mechanisms of tau propagation are largely elusive in 4-repeat tauopathies, characterized not only by neuronal but also by astroglial and oligodendroglial tau accumulation. Here, we assess whether connectivity is associated with 4R-tau deposition patterns by combining resting-state fMRI connectomics with both 2nd generation 18F-PI-2620 tau-PET in 46 patients with clinically diagnosed 4-repeat tauopathies and post-mortem cell-type-specific regional tau assessments from two independent progressive supranuclear palsy patient samples (n = 97 and n = 96). We find that inter-regional connectivity is associated with higher inter-regional correlation of both tau-PET and post-mortem tau levels in 4-repeat tauopathies. In regional cell-type specific post-mortem tau assessments, this association is stronger for neuronal than for astroglial or oligodendroglial tau, suggesting that connectivity is primarily associated with neuronal tau accumulation. Using tau-PET we find further that patient-level tau patterns are associated with the connectivity of subcortical tau epicenters. Together, the current study provides combined in vivo tau-PET and histopathological evidence that brain connectivity is associated with tau deposition patterns in 4-repeat tauopathies.

Published
2022

15. Genome-wide analyses as part of the international FTLD-TDP whole-genome sequencing consortium reveals novel disease risk factors and increases support for immune dysfunction in FTLD

Author

Pottier, Cyril, Ren, Yingxue, Perkerson, Ralph B, Baker, Matt, Jenkins, Gregory D, van Blitterswijk, Marka, DeJesus-Hernandez, Mariely, van Rooij, Jeroen GJ, Murray, Melissa E, Christopher, Elizabeth, McDonnell, Shannon K, Fogarty, Zachary, Batzler, Anthony, Tian, Shulan, Vicente, Cristina T, Matchett, Billie, Karydas, Anna M, Hsiung, Ging-Yuek Robin, Seelaar, Harro, Mol, Merel O, Finger, Elizabeth C, Graff, Caroline, Öijerstedt, Linn, Neumann, Manuela, Heutink, Peter, Synofzik, Matthis, Wilke, Carlo, Prudlo, Johannes, Rizzu, Patrizia, Simon-Sanchez, Javier, Edbauer, Dieter, Roeber, Sigrun, Diehl-Schmid, Janine, Evers, Bret M, King, Andrew, Mesulam, M Marsel, Weintraub, Sandra, Geula, Changiz, Bieniek, Kevin F, Petrucelli, Leonard, Ahern, Geoffrey L, Reiman, Eric M, Woodruff, Bryan K, Caselli, Richard J, Huey, Edward D, Farlow, Martin R, Grafman, Jordan, Mead, Simon, Grinberg, Lea T, Spina, Salvatore, Grossman, Murray, Irwin, David J, Lee, Edward B, Suh, EunRan, Snowden, Julie, Mann, David, Ertekin-Taner, Nilufer, Uitti, Ryan J, Wszolek, Zbigniew K, Josephs, Keith A, Parisi, Joseph E, Knopman, David S, Petersen, Ronald C, Hodges, John R, Piguet, Olivier, Geier, Ethan G, Yokoyama, Jennifer S, Rissman, Robert A, Rogaeva, Ekaterina, Keith, Julia, Zinman, Lorne, Tartaglia, Maria Carmela, Cairns, Nigel J, Cruchaga, Carlos, Ghetti, Bernardino, Kofler, Julia, Lopez, Oscar L, Beach, Thomas G, Arzberger, Thomas, Herms, Jochen, Honig, Lawrence S, Vonsattel, Jean Paul, Halliday, Glenda M, Kwok, John B, White, Charles L, Gearing, Marla, Glass, Jonathan, Rollinson, Sara, Pickering-Brown, Stuart, Rohrer, Jonathan D, Trojanowski, John Q, Van Deerlin, Vivianna, Bigio, Eileen H, Troakes, Claire, Al-Sarraj, Safa, Asmann, Yan, Miller, Bruce L, Graff-Radford, Neill R, Boeve, Bradley F, and Seeley, William W

Subjects
Biomedical and Clinical Sciences, Neurosciences, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Clinical Research, Brain Disorders, Rare Diseases, Human Genome, Alzheimer's Disease Related Dementias (ADRD), Dementia, Prevention, Genetics, Frontotemporal Dementia (FTD), Neurodegenerative, Acquired Cognitive Impairment, Biotechnology, Aetiology, 2.1 Biological and endogenous factors, Aged, DNA Repeat Expansion, Dipeptidyl-Peptidases and Tripeptidyl-Peptidases, Female, Frontal Lobe, Frontotemporal Lobar Degeneration, Genetic Predisposition to Disease, Genome-Wide Association Study, HLA-DQ Antigens, Humans, Intracellular Signaling Peptides and Proteins, Loss of Function Mutation, Male, Middle Aged, Nerve Tissue Proteins, Potassium Channels, Progranulins, Protein Serine-Threonine Kinases, Proteins, RNA, Messenger, Risk Factors, Sequence Analysis, RNA, Societies, Scientific, TDP-43 Proteinopathies, White People, Whole-genome sequencing FTLD-TDP, TBK1, DPP6, UNC13A, HLA, Immunity, Clinical Sciences, Neurology & Neurosurgery
Abstract

Frontotemporal lobar degeneration with neuronal inclusions of the TAR DNA-binding protein 43 (FTLD-TDP) represents the most common pathological subtype of FTLD. We established the international FTLD-TDP whole-genome sequencing consortium to thoroughly characterize the known genetic causes of FTLD-TDP and identify novel genetic risk factors. Through the study of 1131 unrelated Caucasian patients, we estimated that C9orf72 repeat expansions and GRN loss-of-function mutations account for 25.5% and 13.9% of FTLD-TDP patients, respectively. Mutations in TBK1 (1.5%) and other known FTLD genes (1.4%) were rare, and the disease in 57.7% of FTLD-TDP patients was unexplained by the known FTLD genes. To unravel the contribution of common genetic factors to the FTLD-TDP etiology in these patients, we conducted a two-stage association study comprising the analysis of whole-genome sequencing data from 517 FTLD-TDP patients and 838 controls, followed by targeted genotyping of the most associated genomic loci in 119 additional FTLD-TDP patients and 1653 controls. We identified three genome-wide significant FTLD-TDP risk loci: one new locus at chromosome 7q36 within the DPP6 gene led by rs118113626 (p value = 4.82e - 08, OR = 2.12), and two known loci: UNC13A, led by rs1297319 (p value = 1.27e - 08, OR = 1.50) and HLA-DQA2 led by rs17219281 (p value = 3.22e - 08, OR = 1.98). While HLA represents a locus previously implicated in clinical FTLD and related neurodegenerative disorders, the association signal in our study is independent from previously reported associations. Through inspection of our whole-genome sequence data for genes with an excess of rare loss-of-function variants in FTLD-TDP patients (n ≥ 3) as compared to controls (n = 0), we further discovered a possible role for genes functioning within the TBK1-related immune pathway (e.g., DHX58, TRIM21, IRF7) in the genetic etiology of FTLD-TDP. Together, our study based on the largest cohort of unrelated FTLD-TDP patients assembled to date provides a comprehensive view of the genetic landscape of FTLD-TDP, nominates novel FTLD-TDP risk loci, and strongly implicates the immune pathway in FTLD-TDP pathogenesis.

Published
2019

16. 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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17. Adrenal tropism of SARS-CoV-2 and adrenal findings in a post-mortem case series of patients with severe fatal COVID-19

Author

Paul, Tanja, Ledderose, Stephan, Bartsch, Harald, Sun, Na, Soliman, Sarah, Märkl, Bruno, Ruf, Viktoria, Herms, Jochen, Stern, Marcel, Keppler, Oliver T., Delbridge, Claire, Müller, Susanna, Piontek, Guido, Kimoto, Yuki Schneider, Schreiber, Franziska, Williams, Tracy Ann, Neumann, Jens, Knösel, Thomas, Schulz, Heiko, Spallek, Ria, Graw, Matthias, Kirchner, Thomas, Walch, Axel, and Rudelius, Martina

Published
2022
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20. Microglial activation in the right amygdala-entorhinal-hippocampal complex is associated with preserved spatial learning in AppNL-G-F mice

Author

Biechele, Gloria, Wind, Karin, Blume, Tanja, Sacher, Christian, Beyer, Leonie, Eckenweber, Florian, Franzmeier, Nicolai, Ewers, Michael, Zott, Benedikt, Lindner, Simon, Gildehaus, Franz-Josef, von Ungern-Sternberg, Barbara, Tahirovic, Sabina, Willem, Michael, Bartenstein, Peter, Cumming, Paul, Rominger, Axel, Herms, Jochen, and Brendel, Matthias

Published
2021
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21. Deciphering sources of PET signals in the tumor microenvironment of glioblastoma at cellular resolution

Author

Bartos, Laura M., primary, Kirchleitner, Sabrina V., additional, Kolabas, Zeynep Ilgin, additional, Quach, Stefanie, additional, Beck, Alexander, additional, Lorenz, Julia, additional, Blobner, Jens, additional, Mueller, Stephan A., additional, Ulukaya, Selin, additional, Hoeher, Luciano, additional, Horvath, Izabela, additional, Wind-Mark, Karin, additional, Holzgreve, Adrien, additional, Ruf, Viktoria C., additional, Gold, Lukas, additional, Kunze, Lea H., additional, Kunte, Sebastian T., additional, Beumers, Philipp, additional, Park, Ha Eun, additional, Antons, Melissa, additional, Zatcepin, Artem, additional, Briel, Nils, additional, Hoermann, Leonie, additional, Schaefer, Rebecca, additional, Messerer, Denise, additional, Bartenstein, Peter, additional, Riemenschneider, Markus J., additional, Lindner, Simon, additional, Ziegler, Sibylle, additional, Herms, Jochen, additional, Lichtenthaler, Stefan F., additional, Ertürk, Ali, additional, Tonn, Joerg C., additional, von Baumgarten, Louisa, additional, Albert, Nathalie L., additional, and Brendel, Matthias, additional

Published
2023
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26. Prognostic Value of TSPO PET Before Radiotherapy in Newly Diagnosed IDH–Wild-Type Glioblastoma

Author

Albert, Nathalie L., primary, Nelwan, Debie V., additional, Fleischmann, Daniel F., additional, Quach, Stefanie, additional, von Rohr, Katharina, additional, Kaiser, Lena, additional, Teske, Nico, additional, Unterrainer, Lena M., additional, Bartos, Laura M., additional, Ruf, Viktoria C., additional, Brendel, Matthias, additional, Riemenschneider, Markus J., additional, Wetzel, Christian, additional, Herms, Jochen, additional, Rupprecht, Rainer, additional, Thon, Niklas, additional, Tonn, Joerg-Christian, additional, Belka, Claus, additional, Bartenstein, Peter, additional, von Baumgarten, Louisa, additional, Niyazi, Maximilian, additional, Unterrainer, Marcus, additional, and Holzgreve, Adrien, additional

Published
2023
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29. Glial activation is moderated by sex in response to amyloidosis but not to tau pathology in mouse models of neurodegenerative diseases

Author

Biechele, Gloria, Franzmeier, Nicolai, Blume, Tanja, Ewers, Michael, Luque, Jose Medina, Eckenweber, Florian, Sacher, Christian, Beyer, Leonie, Ruch-Rubinstein, Francois, Lindner, Simon, Gildehaus, Franz-Josef, von Ungern-Sternberg, Barbara, Cumming, Paul, Bartenstein, Peter, Rominger, Axel, Höglinger, Günter U., Herms, Jochen, and Brendel, Matthias

Published
2020
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31. Multiple Events Lead to Dendritic Spine Loss in Triple Transgenic Alzheimer's Disease Mice

Author

Bittner, Tobias, Fuhrmann, Martin, Burgold, Steffen, Ochs, Simon M., Hoffmann, Nadine, Mitteregger, Gerda, Kretzschmar, Hans, LaFerla, Frank M., and Herms, Jochen

Subjects
amyloid-precursor-protein, neocortex in-vivo, a-beta, synapse loss, long-term, neurofibrillary tangles, mouse model, cognitive impairment, senile plaques, adult cortex
Abstract

The pathology of Alzheimer's disease (AD) is characterized by the accumulation of amyloid-β (Aβ) peptide, hyperphosphorylated tau protein, neuronal death, and synaptic loss. By means of long-term two-photon in vivo imaging and confocal imaging, we characterized the spatio-temporal pattern of dendritic spine loss for the first time in 3xTg-AD mice. These mice exhibit an early loss of layer III neurons at 4 months of age, at a time when only soluble Aβ is abundant. Later on, dendritic spines are lost around amyloid plaques once they appear at 13 months of age. At the same age, we observed spine loss also in areas apart from amyloid plaques. This plaque independent spine loss manifests exclusively at dystrophic dendrites that accumulate both soluble Aβ and hyperphosphorylated tau intracellularly. Collectively, our data shows that three spatio-temporally independent events contribute to a net loss of dendritic spines. These events coincided either with the occurrence of intracellular soluble or extracellular fibrillar Aβ alone, or the combination of intracellular soluble Aβ and hyperphosphorylated tau.

Published
2010

32. Long-Term Pioglitazone Treatment Has No Significant Impact on Microglial Activation and Tau Pathology in P301S Mice

Author

Kunze, Lea Helena, primary, Ruch, François, additional, Biechele, Gloria, additional, Eckenweber, Florian, additional, Wind-Mark, Karin, additional, Dinkel, Lina, additional, Feyen, Paul, additional, Bartenstein, Peter, additional, Ziegler, Sibylle, additional, Paeger, Lars, additional, Tahirovic, Sabina, additional, Herms, Jochen, additional, and Brendel, Matthias, additional

Published
2023
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33. Longitudinal TSPO expression in tau transgenic P301S mice predicts increased tau accumulation and deteriorated spatial learning

Author

Eckenweber, Florian, Medina-Luque, Jose, Blume, Tanja, Sacher, Christian, Biechele, Gloria, Wind, Karin, Deussing, Maximilian, Briel, Nils, Lindner, Simon, Boening, Guido, von Ungern-Sternberg, Barbara, Unterrainer, Marcus, Albert, Nathalie L., Zwergal, Andreas, Levin, Johannes, Bartenstein, Peter, Cumming, Paul, Rominger, Axel, Höglinger, Günter U., Herms, Jochen, and Brendel, Matthias

Published
2020
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34. Late-stage Anle138b treatment ameliorates tau pathology and metabolic decline in a mouse model of human Alzheimer’s disease tau

Author

Brendel, Matthias, Deussing, Maximilian, Blume, Tanja, Kaiser, Lena, Probst, Federico, Overhoff, Felix, Peters, Finn, von Ungern-Sternberg, Barbara, Ryazanov, Sergey, Leonov, Andrei, Griesinger, Christian, Zwergal, Andreas, Levin, Johannes, Bartenstein, Peter, Yakushev, Igor, Cumming, Paul, Boening, Guido, Ziegler, Sibylle, Herms, Jochen, Giese, Armin, and Rominger, Axel

Published
2019
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36. NIMG-26. UPTAKE OF [18F]GE-180 IN TSPO PET IS ASSOCIATED WITH SURVIVAL IN PATIENTS WITH RECURRENT GLIOMA

Author

Quach, Stefanie, primary, Holzgreve, Adrien, additional, Kaiser, Lena, additional, Unterrainer, Marcus, additional, Dekorsy, Franziska, additional, Nelwan, Debie V, additional, Bartos, Laura, additional, Kirchleitner, Sabrina, additional, Weller, Jonathan, additional, Weidner, Lorraine, additional, Niyazi, Maximilian, additional, Ruf, Victoria, additional, Herms, Jochen, additional, Stöcklein, Sophia, additional, Wetzel, Christian, additional, Riemenschneider, Markus J, additional, von Baumgarten, Louisa, additional, Thon, Niklas, additional, Brendel, Matthias, additional, Rupprecht, Rainer, additional, Bartenstein, Peter, additional, Tonn, Joerg-Christian, additional, and Albert, Nathalie, additional

Published
2022
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37. Improved pasireotide response in USP8 mutant corticotroph tumours in vitro

Author

Albani, Adriana, primary, Perez-Rivas, Luis Gustavo, additional, Tang, Sicheng, additional, Simon, Julia, additional, Lucia, Kristin Elisabeth, additional, Colón-Bolea, Paula, additional, Schopohl, Jochen, additional, Roeber, Sigrun, additional, Buchfelder, Michael, additional, Rotermund, Roman, additional, Flitsch, Jörg, additional, Thorsteinsdottir, Jun, additional, Herms, Jochen, additional, Stalla, Günter, additional, Reincke, Martin, additional, and Theodoropoulou, Marily, additional

Published
2022
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39. A multiplex pedigree with pathologically confirmed multiple system atrophy and Parkinson’s disease with dementia

Author

Fanciulli, Alessandra, primary, Leys, Fabian, additional, Lehner, Fabienne, additional, Sidoroff, Victoria, additional, Ruf, Viktoria C, additional, Raccagni, Cecilia, additional, Mahlknecht, Philipp, additional, Kuipers, Demy J S, additional, van IJcken, Wilfred F J, additional, Stockner, Heike, additional, Musacchio, Thomas, additional, Volkmann, Jens, additional, Monoranu, Camelia Maria, additional, Stankovic, Iva, additional, Breedveld, Guido, additional, Ferraro, Federico, additional, Fevga, Christina, additional, Windl, Otto, additional, Herms, Jochen, additional, Kiechl, Stefan, additional, Poewe, Werner, additional, Seppi, Klaus, additional, Stefanova, Nadia, additional, Scholz, Sonja W, additional, Bonifati, Vincenzo, additional, and Wenning, Gregor K, additional

Published
2022
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43. η-secretase processing of APP inhibits neuronal activity in the hippocampus

Author

Willem, Michael, Tahirovic, Sabina, Busche, Marc Aurel, Ovsepian, Saak V., Chafai, Magda, Kootar, Scherazad, Hornburg, Daniel, Evans, Lewis D.B., Moore, Steven, Daria, Anna, Hampel, Heike, Muller, Veronika, Giudici, Camilla, Nuscher, Brigitte, Wenninger-Weinzierl, Andrea, Kremmer, Elisabeth, Heneka, Michael T., Thal, Dietmar R., Giedraitis, Vilmantas, Lannfelt, Lars, Muller, Ulrike, Livesey, Frederick J., Meissner, Felix, Herms, Jochen, Konnerth, Arthur, Marie, Helene, and Haass, Christian

Subjects
Hippocampus (Brain) -- Health aspects, Neural circuitry -- Health aspects, Proteases -- Health aspects, Amyloid beta-protein -- Health aspects, Alzheimer's disease -- Physiological aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Alzheimer disease (AD) is characterized by the accumulation of amyloid plaques, which are predominantly composed of amyloid-β peptide (1). Two principal physiological pathways either prevent or promote amyloid-β generation from its precursor, β-amyloid precursor protein (APP), in a competitive manner (1). Although APP processing has been studied in great detail, unknown proteolytic events seem to hinder stoichiometric analyses of APP metabolism in vivo (2). Here we describe a new physiological APP processing pathway, which generates proteolytic fragments capable of inhibiting neuronal activity within the hippocampus. We identify higher molecular mass carboxy-terminal fragments (CTFs) of APP, termed CTF-η, in addition to the long-known CTF-α and CTF-β fragments generated by the α- and β-secretases ADAM10 (a disintegrin and metalloproteinase 10) and BACE1 (β-site APP cleaving enzyme 1), respectively. CTF-η generation is mediated in part by membrane-bound matrix metalloproteinases such as MT5-MMP, referred to as η-secretase activity. η-Secretase cleavage occurs primarily at amino acids 504-505 of [APP.sub.695], releasing a truncated ectodomain. After shedding of this ectodomain, CTF-η is further processed by ADAM10 and BACE1 to release long and short Aη peptides (termed Aη-α and Aη-β). CTFs produced by η-secretase are enriched in dystrophic neurites in an AD mouse model and in human AD brains. Genetic and pharmacological inhibition of BACE1 activity results in robust accumulation of CTF-η and Aη-α. In mice treated with a potent BACE1 inhibitor, hippocampal long-term potentiation was reduced. Notably, when recombinant or synthetic Aη-α was applied on hippocampal slices exvivo, long-term potentiation was lowered. Furthermore, in vivo single-cell two-photon calcium imaging showed that hippocampal neuronal activity was attenuated by Aη-α. These findings not only demonstrate a major functionally relevant APP processing pathway, but may also indicate potential translational relevance for therapeutic strategies targeting APP processing., To identify new proteolytic pathways of APP, we searched for CTFs other than those giving rise to P3 fragment (CTF-α) or amyloid-β (CTF-β) (3-5). A new CTF with an approximate [...]

Published
2015

44. PATH-04. Array-based global DNA Methylation profiling of mouse brain tumors allows comparison to human tumors

Author

Schoof, Melanie, primary, Spohn, Michael, additional, Dorostkar, Mario, additional, Neyazi, Sina, additional, Bockmayr, Michael, additional, Swartling, Fredrik, additional, Kawauchi, Daisuke, additional, Gilbertson, Richard, additional, Taylor, Jessica, additional, Pei, Yanxin, additional, Glass, Rainer, additional, Cheng, Jiying, additional, Galarza, Natalia Moreno, additional, Hench, Juergen, additional, Herms, Jochen, additional, Jurmeister, Philipp, additional, Schweizer, Leonille, additional, Capper, David, additional, Harter, Patrick, additional, Thomas, Christian, additional, Hasselblatt, Martin, additional, Blattner-Johnson, Mirjam, additional, Jones, David, additional, Frank, Stephan, additional, Kerl, Kornelius, additional, and Schüller, Ulrich, additional

Published
2022
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45. 18F-PI-2620 Tau PET Improves the Imaging Diagnosis of Progressive Supranuclear Palsy

Author

Messerschmidt, Konstantin, primary, Barthel, Henryk, additional, Brendel, Matthias, additional, Scherlach, Cordula, additional, Hoffmann, Karl-Titus, additional, Rauchmann, Boris-Stephan, additional, Rullmann, Michael, additional, Marek, Kenneth, additional, Villemagne, Victor L., additional, Rumpf, Jost-Julian, additional, Saur, Dorothee, additional, Schroeter, Matthias L., additional, Schildan, Andreas, additional, Patt, Marianne, additional, Beyer, Leonie, additional, Song, Mengmeng, additional, Palleis, Carla, additional, Katzdobler, Sabrina, additional, Fietzek, Urban M., additional, Respondek, Gesine, additional, Scheifele, Maximilian, additional, Nitschmann, Alexander, additional, Zach, Christian, additional, Barret, Olivier, additional, Madonia, Jennifer, additional, Russell, David, additional, Stephens, Andrew W, additional, Koglin, Norman, additional, Roeber, Sigrun, additional, Herms, Jochen, additional, Boetzel, Kai, additional, Bartenstein, Peter, additional, Levin, Johannes, additional, Seibyl, John P., additional, Höglinger, Günter, additional, Classen, Joseph, additional, and Sabri, Osama, additional

Published
2022
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46. Additional file 1 of 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

Abstract

Additional file 1. Supplementary Table 1: Description of study cohort. Supplementary Table 2: Primers used for TP53 amplification and Sanger sequencing. Supplementary Table 3: Common TP53 variants in the study cohort. Supplementary Table 4: Comparison of TP53 mutant versus TP53 wild type group. Supplementary Figure 1. Chromatograms showing the TP53 variants found in the corticotroph tumor of patient #1 and #8 (Table 1). A. The variant c.398T>A was present in homozygocity in the tumor and absent in the blood. B. The variant c.1009C>G is detected in all available surgical specimens in this patient. First and 2nd surgeries were Cushing’s disease tumors and 4th and 5th CTP-BADX/NS.

Published
2022
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47. Glitter in the Darkness? Non-fibrillar ��-amyloid Plaque Components Significantly Impact the ��-amyloid PET Signal in Mouse Models of Alzheimer's Disease

Author

Biechele, Gloria, Sebastian Monasor, Laura, Wind, Karin, Blume, Tanja, Parhizkar, Samira, Arzberger, Thomas, Sacher, Christian, Beyer, Leonie, Eckenweber, Florian, Gildehaus, Franz-Josef, von Ungern-Sternberg, Barbara, Willem, Michael, Bartenstein, Peter, Cumming, Paul, Rominger, Axel, Herms, Jochen, Lichtenthaler, Stefan, Haass, Christian, Tahirovic, Sabina, and Brendel, Matthias

Subjects
macromolecular substances, 610 Medicine & health
Abstract

Objective: ��-amyloid PET (A��-PET) is an important tool for quantification of amyloidosis in the brain of suspected Alzheimer's disease (AD) patients and transgenic AD mouse models. Despite the excellent correlation of A��-PET with gold standard immunohistochemical assessments, the relative contributions of fibrillar and non-fibrillar A�� components to the in vivo A��-PET signal remain unclear. Thus, we obtained two murine cerebral amyloidosis models that present with distinct A�� plaque compositions and performed regression analysis between immunohistochemistry and A�� PET to determine the biochemical contributions to A��-PET signal in vivo. Methods: We investigated groups of AppNL-G-F and APPPS1 mice at three, six and 12 months of age by longitudinal 18F-florbetaben A��-PET and with immunohistochemical analysis of the fibrillar and total A�� burdens. We then applied group level inter-modality regression models using age and genotype matched sets of fibrillar/ non-fibrillar A�� data (predictors) and A��-PET results (outcome) for both transgenic models. An independent group of double-hit APPPS1 mice with dysfunctional microglia due to knock-out of triggering receptor expression on myeloid cells 2 (Trem2-/-) served for validation and evaluation of translational impact. Results: Neither fibrillar nor non-fibrillar A�� content alone sufficed to explain the A��-PET findings in either transgenic AD model. However, a regression model compiling fibrillar and non-fibrillar A�� together with the estimate of individual heterogeneity and age at scanning could explain a 93% of variance of the A��-PET signal (P

Published
2022
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48. Chronic PPARγ Stimulation Shifts Amyloidosis to Higher Fibrillarity but Improves Cognition

Author

Blume, Tanja, primary, Deussing, Maximilian, additional, Biechele, Gloria, additional, Peters, Finn, additional, Zott, Benedikt, additional, Schmidt, Claudio, additional, Franzmeier, Nicolai, additional, Wind, Karin, additional, Eckenweber, Florian, additional, Sacher, Christian, additional, Shi, Yuan, additional, Ochs, Katharina, additional, Kleinberger, Gernot, additional, Xiang, Xianyuan, additional, Focke, Carola, additional, Lindner, Simon, additional, Gildehaus, Franz-Josef, additional, Beyer, Leonie, additional, von Ungern-Sternberg, Barbara, additional, Bartenstein, Peter, additional, Baumann, Karlheinz, additional, Adelsberger, Helmuth, additional, Rominger, Axel, additional, Cumming, Paul, additional, Willem, Michael, additional, Dorostkar, Mario M., additional, Herms, Jochen, additional, and Brendel, Matthias, additional

Published
2022
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49. Long-Duration Progressive Supranuclear Palsy: Clinical Course and Pathological Underpinnings

Author

Jecmenica Lukic, Milica, Respondek, Gesine, Giese, Armin, Roeber, Sigrun, Herms, Jochen, Arzberger, Thomas, Höglinger, Günter, Troakes, Claire, Gelpi, Ellen, Höglinger, Günter U, Kurz, Carolin, van Swieten, John, Compta, Yaroslau, Molina-Porcel, L., Aldecoa, I., Tolosa, E., Martí, M. J., Valldeoriola, F., Pagonabarraga, J., Calopa, M., Bayès, A., Hernandez, I., Aguilar, M., Genis, D., Ferguson, Leslie W, Rajput, Alex, group, MDS-endorsed PSP study, van Swieten, John C, and Neurology

Subjects
Neurons, metabolism [Astrocytes], pathology [Supranuclear Palsy, Progressive], tau Proteins, metabolism [tau Proteins], ddc, Research Article, Research Articles, Neurology, metabolism [Neurons], Astrocytes, Disease Progression, Humans, Neurology (clinical), ddc:610, Autopsy, Supranuclear Palsy, Progressive
Abstract

Objectives: To identify the clinical characteristics of the subgroup of benign progressive supranuclear palsy with particularly long disease duration; to define neuropathological determinants underlying variability in disease duration in progressive supranuclear palsy. Methods: Clinical and pathological features were compared among 186 autopsy-confirmed cases with progressive supranuclear palsy with ≥10 years and shorter survival times. Results: The 45 cases (24.2%) had a disease duration of ≥10 years. The absence of ocular motor abnormalities within the first 3 years from disease onset was the only significant independent clinical predictor of longer survival. Histopathologically, the neurodegeneration parameters in each survival group were paralleled anatomically by the distribution of neuronal cytoplasmic inclusions, whereas the tufted astrocytes displayed anatomically an opposite severity pattern. Most interestingly, we found significantly less coiled bodies in those who survive longer, in contrast to patients with less favorable course. Interpretation: A considerable proportion of patients had a more ”benign” disease course with ≥10 years survival. They had a distinct pattern and evolution of core symptoms compared to patients with short survival. The inverted anatomical patterns of astrocytic tau distribution suggest distinct implications of these cell types in trans-cellular propagation. The tempo of disease progression appeared to be determined mostly by oligodendroglial tau, where the high degree of oligodendroglial tau pathology might affect neuronal integrity and function on top of neuronal tau pathology. The relative contribution of glial tau should be further explored in cellular and animal models. ANN NEUROL 2022.

Published
2021

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