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1. Blood-based quantification of Aβ oligomers indicates impaired clearance from brain in ApoE ε4 positive subjects

Author

Blömeke, Lara, Rehn, Fabian, Pils, Marlene, Kraemer-Schulien, Victoria, Cousin, Anneliese, Kutzsche, Janine, Bujnicki, Tuyen, Freiesleben, Silka D., Schneider, Luisa-Sophie, Preis, Lukas, Priller, Josef, Spruth, Eike J., Altenstein, Slawek, Schneider, Anja, Fliessbach, Klaus, Wiltfang, Jens, Hansen, Niels, Rostamzadeh, Ayda, Düzel, Emrah, Glanz, Wenzel, Incesoy, Enise I., Buerger, Katharina, Janowitz, Daniel, Ewers, Michael, Perneczky, Robert, Rauchmann, Boris-Stephan, Teipel, Stefan, Kilimann, Ingo, Laske, Christoph, Munk, Matthias H., Spottke, Annika, Roy, Nina, Heneka, Michael T., Brosseron, Frederic, Wagner, Michael, Roeske, Sandra, Ramirez, Alfredo, Schmid, Matthias, Jessen, Frank, Bannach, Oliver, Peters, Oliver, and Willbold, Dieter

Published
2024
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2. Cognitive reserve against Alzheimer’s pathology is linked to brain activity during memory formation

Author

Vockert, Niklas, Machts, Judith, Kleineidam, Luca, Nemali, Aditya, Incesoy, Enise I., Bernal, Jose, Schütze, Hartmut, Yakupov, Renat, Peters, Oliver, Gref, Daria, Schneider, Luisa Sophie, Preis, Lukas, Priller, Josef, Spruth, Eike Jakob, Altenstein, Slawek, Schneider, Anja, Fliessbach, Klaus, Wiltfang, Jens, Rostamzadeh, Ayda, Glanz, Wenzel, Teipel, Stefan, Kilimann, Ingo, Goerss, Doreen, Laske, Christoph, Munk, Matthias H., Spottke, Annika, Roy, Nina, Heneka, Michael T., Brosseron, Frederic, Wagner, Michael, Wolfsgruber, Steffen, Dobisch, Laura, Dechent, Peter, Hetzer, Stefan, Scheffler, Klaus, Zeidman, Peter, Stern, Yaakov, Schott, Björn H., Jessen, Frank, Düzel, Emrah, Maass, Anne, and Ziegler, Gabriel

Published
2024
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3. Perivascular space enlargement accelerates in ageing and Alzheimer’s disease pathology: evidence from a three-year longitudinal multicentre study

Author

Menze, Inga, Bernal, Jose, Kaya, Pinar, Aki, Çağla, Pfister, Malte, Geisendörfer, Jonas, Yakupov, Renat, Coello, Roberto Duarte, Valdés-Hernández, Maria d. C., Heneka, Michael T., Brosseron, Frederic, Schmid, Matthias C., Glanz, Wenzel, Incesoy, Enise I., Butryn, Michaela, Rostamzadeh, Ayda, Meiberth, Dix, Peters, Oliver, Preis, Lukas, Lammerding, Dominik, Gref, Daria, Priller, Josef, Spruth, Eike J., Altenstein, Slawek, Lohse, Andrea, Hetzer, Stefan, Schneider, Anja, Fliessbach, Klaus, Kimmich, Okka, Vogt, Ina R., Wiltfang, Jens, Bartels, Claudia, Schott, Björn H., Hansen, Niels, Dechent, Peter, Buerger, Katharina, Janowitz, Daniel, Perneczky, Robert, Rauchmann, Boris-Stephan, Teipel, Stefan, Kilimann, Ingo, Goerss, Doreen, Laske, Christoph, Munk, Matthias H., Sanzenbacher, Carolin, Hinderer, Petra, Scheffler, Klaus, Spottke, Annika, Roy-Kluth, Nina, Lüsebrink, Falk, Neumann, Katja, Wardlaw, Joanna, Jessen, Frank, Schreiber, Stefanie, Düzel, Emrah, and Ziegler, Gabriel

Published
2024
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6. 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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8. Microglia states and nomenclature: A field at its crossroads

Author

Paolicelli, Rosa C, Sierra, Amanda, Stevens, Beth, Tremblay, Marie-Eve, Aguzzi, Adriano, Ajami, Bahareh, Amit, Ido, Audinat, Etienne, Bechmann, Ingo, Bennett, Mariko, Bennett, Frederick, Bessis, Alain, Biber, Knut, Bilbo, Staci, Blurton-Jones, Mathew, Boddeke, Erik, Brites, Dora, Brône, Bert, Brown, Guy C, Butovsky, Oleg, Carson, Monica J, Castellano, Bernardo, Colonna, Marco, Cowley, Sally A, Cunningham, Colm, Davalos, Dimitrios, De Jager, Philip L, de Strooper, Bart, Denes, Adam, Eggen, Bart JL, Eyo, Ukpong, Galea, Elena, Garel, Sonia, Ginhoux, Florent, Glass, Christopher K, Gokce, Ozgun, Gomez-Nicola, Diego, González, Berta, Gordon, Siamon, Graeber, Manuel B, Greenhalgh, Andrew D, Gressens, Pierre, Greter, Melanie, Gutmann, David H, Haass, Christian, Heneka, Michael T, Heppner, Frank L, Hong, Soyon, Hume, David A, Jung, Steffen, Kettenmann, Helmut, Kipnis, Jonathan, Koyama, Ryuta, Lemke, Greg, Lynch, Marina, Majewska, Ania, Malcangio, Marzia, Malm, Tarja, Mancuso, Renzo, Masuda, Takahiro, Matteoli, Michela, McColl, Barry W, Miron, Veronique E, Molofsky, Anna Victoria, Monje, Michelle, Mracsko, Eva, Nadjar, Agnes, Neher, Jonas J, Neniskyte, Urte, Neumann, Harald, Noda, Mami, Peng, Bo, Peri, Francesca, Perry, V Hugh, Popovich, Phillip G, Pridans, Clare, Priller, Josef, Prinz, Marco, Ragozzino, Davide, Ransohoff, Richard M, Salter, Michael W, Schaefer, Anne, Schafer, Dorothy P, Schwartz, Michal, Simons, Mikael, Smith, Cody J, Streit, Wolfgang J, Tay, Tuan Leng, Tsai, Li-Huei, Verkhratsky, Alexei, von Bernhardi, Rommy, Wake, Hiroaki, Wittamer, Valérie, Wolf, Susanne A, Wu, Long-Jun, and Wyss-Coray, Tony

Subjects
Microglia, Neurosciences, Psychology, Cognitive Sciences, Neurology & Neurosurgery
Abstract

Microglial research has advanced considerably in recent decades yet has been constrained by a rolling series of dichotomies such as "resting versus activated" and "M1 versus M2." This dualistic classification of good or bad microglia is inconsistent with the wide repertoire of microglial states and functions in development, plasticity, aging, and diseases that were elucidated in recent years. New designations continuously arising in an attempt to describe the different microglial states, notably defined using transcriptomics and proteomics, may easily lead to a misleading, although unintentional, coupling of categories and functions. To address these issues, we assembled a group of multidisciplinary experts to discuss our current understanding of microglial states as a dynamic concept and the importance of addressing microglial function. Here, we provide a conceptual framework and recommendations on the use of microglial nomenclature for researchers, reviewers, and editors, which will serve as the foundations for a future white paper.

Published
2022

9. Impact of COVID‐19 on the Onset and Progression of Alzheimer's Disease and Related Dementias: A Roadmap for Future Research

Author

Gordon, Marcia N, Heneka, Michael T, Le Page, Lydia M, Limberger, Christian, Morgan, David, Tenner, Andrea J, Terrando, Niccolò, Willette, Auriel A, and Willette, Sara A

Subjects
Biomedical and Clinical Sciences, Biological Psychology, Clinical Sciences, Neurosciences, Psychology, Acquired Cognitive Impairment, Infectious Diseases, Clinical Research, Neurodegenerative, Brain Disorders, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aging, Coronaviruses, Emerging Infectious Diseases, Social Determinants of Health, Dementia, Behavioral and Social Science, Alzheimer's Disease, Coronaviruses Disparities and At-Risk Populations, 2.1 Biological and endogenous factors, Neurological, Good Health and Well Being, Alzheimer Disease, COVID-19, Caregivers, Cognitive Dysfunction, Communicable Disease Control, Humans, Alzheimer's risk factor, caregiver burden, delerium, longitudinal cohort, systemic inflammation, SARS-CoV-2, Geriatrics, Clinical sciences, Biological psychology
Abstract

COVID-19 causes lasting neurological symptoms in some survivors. Like other infections, COVID-19 may increase risk of cognitive impairment. This perspective highlights four knowledge gaps about COVID-19 that need to be filled to avoid this possible health issue. The first is the need to identify the COVID-19 symptoms, genetic polymorphisms and treatment decisions associated with risk of cognitive impairment. The second is the absence of model systems in which to test hypotheses relating infection to cognition. The third is the need for consortia for studying both existing and new longitudinal cohorts in which to monitor long term consequences of COVID-19 infection. A final knowledge gap discussed is the impact of the isolation and lack of social services brought about by quarantine/lockdowns on people living with dementia and their caregivers. Research into these areas may lead to interventions that reduce the overall risk of cognitive decline for COVID-19 survivors.

Published
2022

10. Improving 3D convolutional neural network comprehensibility via interactive visualization of relevance maps: Evaluation in Alzheimer's disease

Author

Dyrba, Martin, Hanzig, Moritz, Altenstein, Slawek, Bader, Sebastian, Ballarini, Tommaso, Brosseron, Frederic, Buerger, Katharina, Cantré, Daniel, Dechent, Peter, Dobisch, Laura, Düzel, Emrah, Ewers, Michael, Fliessbach, Klaus, Glanz, Wenzel, Haynes, John-Dylan, Heneka, Michael T., Janowitz, Daniel, Keles, Deniz B., Kilimann, Ingo, Laske, Christoph, Maier, Franziska, Metzger, Coraline D., Munk, Matthias H., Perneczky, Robert, Peters, Oliver, Preis, Lukas, Priller, Josef, Rauchmann, Boris, Roy, Nina, Scheffler, Klaus, Schneider, Anja, Schott, Björn H., Spottke, Annika, Spruth, Eike J., Weber, Marc-André, Ertl-Wagner, Birgit, Wagner, Michael, Wiltfang, Jens, Jessen, Frank, and Teipel, Stefan J.

Subjects
Electrical Engineering and Systems Science - Image and Video Processing, Computer Science - Computer Vision and Pattern Recognition
Abstract

Background: Although convolutional neural networks (CNN) achieve high diagnostic accuracy for detecting Alzheimer's disease (AD) dementia based on magnetic resonance imaging (MRI) scans, they are not yet applied in clinical routine. One important reason for this is a lack of model comprehensibility. Recently developed visualization methods for deriving CNN relevance maps may help to fill this gap. We investigated whether models with higher accuracy also rely more on discriminative brain regions predefined by prior knowledge. Methods: We trained a CNN for the detection of AD in N=663 T1-weighted MRI scans of patients with dementia and amnestic mild cognitive impairment (MCI) and verified the accuracy of the models via cross-validation and in three independent samples including N=1655 cases. We evaluated the association of relevance scores and hippocampus volume to validate the clinical utility of this approach. To improve model comprehensibility, we implemented an interactive visualization of 3D CNN relevance maps. Results: Across three independent datasets, group separation showed high accuracy for AD dementia vs. controls (AUC$\geq$0.92) and moderate accuracy for MCI vs. controls (AUC$\approx$0.75). Relevance maps indicated that hippocampal atrophy was considered as the most informative factor for AD detection, with additional contributions from atrophy in other cortical and subcortical regions. Relevance scores within the hippocampus were highly correlated with hippocampal volumes (Pearson's r$\approx$-0.86, p<0.001). Conclusion: The relevance maps highlighted atrophy in regions that we had hypothesized a priori. This strengthens the comprehensibility of the CNN models, which were trained in a purely data-driven manner based on the scans and diagnosis labels., Comment: 24 pages, 9 figures/tables, supplementary material, source code available on GitHub

Published
2020
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11. Serum IL-6, sAXL, and YKL-40 as systemic correlates of reduced brain structure and function in Alzheimer’s disease: results from the DELCODE study

Author

Brosseron, Frederic, Maass, Anne, Kleineidam, Luca, Ravichandran, Kishore Aravind, Kolbe, Carl-Christian, Wolfsgruber, Steffen, Santarelli, Francesco, Häsler, Lisa M., McManus, Róisín, Ising, Christina, Röske, Sandra, Peters, Oliver, Cosma, Nicoleta-Carmen, Schneider, Luisa-Sophie, Wang, Xiao, Priller, Josef, Spruth, Eike J., Altenstein, Slawek, Schneider, Anja, Fliessbach, Klaus, Wiltfang, Jens, Schott, Björn H., Buerger, Katharina, Janowitz, Daniel, Dichgans, Martin, Perneczky, Robert, Rauchmann, Boris-Stephan, Teipel, Stefan, Kilimann, Ingo, Görß, Doreen, Laske, Christoph, Munk, Matthias H., Düzel, Emrah, Yakupow, Renat, Dobisch, Laura, Metzger, Coraline D., Glanz, Wenzel, Ewers, Michael, Dechent, Peter, Haynes, John Dylan, Scheffler, Klaus, Roy, Nina, Rostamzadeh, Ayda, Spottke, Annika, Ramirez, Alfredo, Mengel, David, Synofzik, Matthis, Jucker, Mathias, Latz, Eicke, Jessen, Frank, Wagner, Michael, and Heneka, Michael T.

Published
2023
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12. Author Correction: Common variants in Alzheimer’s disease and risk stratification by polygenic risk scores

Author

de Rojas, Itziar, Moreno-Grau, Sonia, Tesi, Niccolo, Grenier-Boley, Benjamin, Andrade, Victor, Jansen, Iris E., Pedersen, Nancy L., Stringa, Najada, Zettergren, Anna, Hernández, Isabel, Montrreal, Laura, Antúnez, Carmen, Antonell, Anna, Tankard, Rick M., Bis, Joshua C., Sims, Rebecca, Bellenguez, Céline, Quintela, Inés, González-Perez, Antonio, Calero, Miguel, Franco-Macías, Emilio, Macías, Juan, Blesa, Rafael, Cervera-Carles, Laura, Menéndez-González, Manuel, Frank-García, Ana, Royo, Jose Luís, Moreno, Fermin, Huerto Vilas, Raquel, Baquero, Miquel, Diez-Fairen, Mónica, Lage, Carmen, García-Madrona, Sebastián, García-González, Pablo, Alarcón-Martín, Emilio, Valero, Sergi, Sotolongo-Grau, Oscar, Ullgren, Abbe, Naj, Adam C., Lemstra, Afina W., Benaque, Alba, Pérez-Cordón, Alba, Benussi, Alberto, Rábano, Alberto, Padovani, Alessandro, Squassina, Alessio, de Mendonça, Alexandre, Arias Pastor, Alfonso, Kok, Almar A. L., Meggy, Alun, Pastor, Ana Belén, Espinosa, Ana, Corma-Gómez, Anaïs, Martín Montes, Angel, Sanabria, Ángela, DeStefano, Anita L., Schneider, Anja, Haapasalo, Annakaisa, Kinhult Ståhlbom, Anne, Tybjærg-Hansen, Anne, Hartmann, Annette M., Spottke, Annika, Corbatón-Anchuelo, Arturo, Rongve, Arvid, Borroni, Barbara, Arosio, Beatrice, Nacmias, Benedetta, Nordestgaard, Børge G., Kunkle, Brian W., Charbonnier, Camille, Abdelnour, Carla, Masullo, Carlo, Martínez Rodríguez, Carmen, Muñoz-Fernandez, Carmen, Dufouil, Carole, Graff, Caroline, Ferreira, Catarina B., Chillotti, Caterina, Reynolds, Chandra A., Fenoglio, Chiara, Van Broeckhoven, Christine, Clark, Christopher, Pisanu, Claudia, Satizabal, Claudia L., Holmes, Clive, Buiza-Rueda, Dolores, Aarsland, Dag, Rujescu, Dan, Alcolea, Daniel, Galimberti, Daniela, Wallon, David, Seripa, Davide, Grünblatt, Edna, Dardiotis, Efthimios, Düzel, Emrah, Scarpini, Elio, Conti, Elisa, Rubino, Elisa, Gelpi, Ellen, Rodriguez-Rodriguez, Eloy, Duron, Emmanuelle, Boerwinkle, Eric, Ferri, Evelyn, Tagliavini, Fabrizio, Küçükali, Fahri, Pasquier, Florence, Sanchez-Garcia, Florentino, Mangialasche, Francesca, Jessen, Frank, Nicolas, Gaël, Selbæk, Geir, Ortega, Gemma, Chêne, Geneviève, Hadjigeorgiou, Georgios, Rossi, Giacomina, Spalletta, Gianfranco, Giaccone, Giorgio, Grande, Giulia, Binetti, Giuliano, Papenberg, Goran, Hampel, Harald, Bailly, Henri, Zetterberg, Henrik, Soininen, Hilkka, Karlsson, Ida K., Alvarez, Ignacio, Appollonio, Ildebrando, Giegling, Ina, Skoog, Ingmar, Saltvedt, Ingvild, Rainero, Innocenzo, Rosas Allende, Irene, Hort, Jakub, Diehl-Schmid, Janine, Van Dongen, Jasper, Vidal, Jean-Sebastien, Lehtisalo, Jenni, Wiltfang, Jens, Thomassen, Jesper Qvist, Kornhuber, Johannes, Haines, Jonathan L., Vogelgsang, Jonathan, Pineda, Juan A., Fortea, Juan, Popp, Julius, Deckert, Jürgen, Buerger, Katharina, Morgan, Kevin, Fließbach, Klaus, Sleegers, Kristel, Molina-Porcel, Laura, Kilander, Lena, Weinhold, Leonie, Farrer, Lindsay A., Wang, Li-San, Kleineidam, Luca, Farotti, Lucia, Parnetti, Lucilla, Tremolizzo, Lucio, Hausner, Lucrezia, Benussi, Luisa, Froelich, Lutz, Ikram, M. Arfan, Deniz-Naranjo, M. Candida, Tsolaki, Magda, Rosende-Roca, Maitée, Löwenmark, Malin, Hulsman, Marc, Spallazzi, Marco, Pericak-Vance, Margaret A., Esiri, Margaret, Bernal Sánchez-Arjona, María, Dalmasso, Maria Carolina, Martínez-Larrad, María Teresa, Arcaro, Marina, Nöthen, Markus M., Fernández-Fuertes, Marta, Dichgans, Martin, Ingelsson, Martin, Herrmann, Martin J., Scherer, Martin, Vyhnalek, Martin, Kosmidis, Mary H., Yannakoulia, Mary, Schmid, Matthias, Ewers, Michael, Heneka, Michael T., Wagner, Michael, Scamosci, Michela, Kivipelto, Miia, Hiltunen, Mikko, Zulaica, Miren, Alegret, Montserrat, Fornage, Myriam, Roberto, Natalia, van Schoor, Natasja M., Seidu, Nazib M., Banaj, Nerisa, Armstrong, Nicola J., Scarmeas, Nikolaos, Scherbaum, Norbert, Goldhardt, Oliver, Hanon, Oliver, Peters, Oliver, Skrobot, Olivia Anna, Quenez, Olivier, Lerch, Ondrej, Bossù, Paola, Caffarra, Paolo, Dionigi Rossi, Paolo, Sakka, Paraskevi, Mecocci, Patrizia, Hoffmann, Per, Holmans, Peter A., Fischer, Peter, Riederer, Peter, Yang, Qiong, Marshall, Rachel, Kalaria, Rajesh N., Mayeux, Richard, Vandenberghe, Rik, Cecchetti, Roberta, Ghidoni, Roberta, Frikke-Schmidt, Ruth, Sorbi, Sandro, Hägg, Sara, Engelborghs, Sebastiaan, Helisalmi, Seppo, Botne Sando, Sigrid, Kern, Silke, Archetti, Silvana, Boschi, Silvia, Fostinelli, Silvia, Gil, Silvia, Mendoza, Silvia, Mead, Simon, Ciccone, Simona, Djurovic, Srdjan, Heilmann-Heimbach, Stefanie, Riedel-Heller, Steffi, Kuulasmaa, Teemu, del Ser, Teodoro, Lebouvier, Thibaud, Polak, Thomas, Ngandu, Tiia, Grimmer, Timo, Bessi, Valentina, Escott-Price, Valentina, Giedraitis, Vilmantas, Deramecourt, Vincent, Maier, Wolfgang, Jian, Xueqiu, Pijnenburg, Yolande A. L., Kehoe, Patrick Gavin, Garcia-Ribas, Guillermo, Sánchez-Juan, Pascual, Pastor, Pau, Pérez-Tur, Jordi, Piñol-Ripoll, Gerard, Lopez de Munain, Adolfo, García-Alberca, Jose María, Bullido, María J., Álvarez, Victoria, Lleó, Alberto, Real, Luis M., Mir, Pablo, Medina, Miguel, Scheltens, Philip, Holstege, Henne, Marquié, Marta, Sáez, María Eugenia, Carracedo, Ángel, Amouyel, Philippe, Schellenberg, Gerard D., Williams, Julie, Seshadri, Sudha, van Duijn, Cornelia M., Mather, Karen A., Sánchez-Valle, Raquel, Serrano-Ríos, Manuel, Orellana, Adelina, Tárraga, Lluís, Blennow, Kaj, Huisman, Martijn, Andreassen, Ole A., Posthuma, Danielle, Clarimón, Jordi, Boada, Mercè, van der Flier, Wiesje M., Ramirez, Alfredo, Lambert, Jean-Charles, van der Lee, Sven J., and Ruiz, Agustín

Published
2023
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13. Exploring the ATN classification system using brain morphology

Author

Heinzinger, Nils, Maass, Anne, Berron, David, Yakupov, Renat, Peters, Oliver, Fiebach, Jochen, Villringer, Kersten, Preis, Lukas, Priller, Josef, Spruth, Eike Jacob, Altenstein, Slawek, Schneider, Anja, Fliessbach, Klaus, Wiltfang, Jens, Bartels, Claudia, Jessen, Frank, Maier, Franziska, Glanz, Wenzel, Buerger, Katharina, Janowitz, Daniel, Perneczky, Robert, Rauchmann, Boris-Stephan, Teipel, Stefan, Killimann, Ingo, Göerß, Doreen, Laske, Christoph, Munk, Matthias H., Spottke, Annika, Roy, Nina, Heneka, Michael T., Brosseron, Frederic, Dobisch, Laura, Ewers, Michael, Dechent, Peter, Haynes, John Dylan, Scheffler, Klaus, Wolfsgruber, Steffen, Kleineidam, Luca, Schmid, Matthias, Berger, Moritz, Düzel, Emrah, and Ziegler, Gabriel

Published
2023
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14. Infection and inflammation: New perspectives on Alzheimer's disease

Author

Aiello, Alison, Chiba-Falek, Ornit, Heitman, Joseph, Johnson, Kim G., Luftig, Micah, Moseman, Ashley, Rawls, Jonathan, Shinohara, Mari L., Swanstrom, Ronald, Terrando, Niccolo, Whitson, Heather E., Colton, Carol, El Khoury, Joseph, Gate, David, Goate, Alison, Heneka, Michael T., Kaddurah-Daouk, Rima, Klein, Robyn S., Sisodia, Sangram, Spudich, Serena S., Stevens, Beth, Tanzi, Rudolph, Ting, Jenny P., and Garden, Gwenn

Published
2022
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16. Soluble TAM receptors sAXL and sTyro3 predict structural and functional protection in Alzheimer’s disease

Author

Brosseron, Frederic, Maass, Anne, Kleineidam, Luca, Ravichandran, Kishore Aravind, González, Pablo García, McManus, Róisín M., Ising, Christina, Santarelli, Francesco, Kolbe, Carl-Christian, Häsler, Lisa M., Wolfsgruber, Steffen, Marquié, Marta, Boada, Mercè, Orellana, Adelina, de Rojas, Itziar, Röske, Sandra, Peters, Oliver, Cosma, Nicoleta-Carmen, Cetindag, Arda, Wang, Xiao, Priller, Josef, Spruth, Eike J., Altenstein, Slawek, Schneider, Anja, Fliessbach, Klaus, Wiltfang, Jens, Schott, Björn H., Bürger, Katharina, Janowitz, Daniel, Dichgans, Martin, Perneczky, Robert, Rauchmann, Boris-Stephan, Teipel, Stefan, Kilimann, Ingo, Goerss, Doreen, Laske, Christoph, Munk, Matthias H., Düzel, Emrah, Yakupov, Renat, Dobisch, Laura, Metzger, Coraline D., Glanz, Wenzel, Ewers, Michael, Dechent, Peter, Haynes, John Dylan, Scheffler, Klaus, Roy, Nina, Rostamzadeh, Ayda, Teunissen, Charlotte E., Marchant, Natalie L., Spottke, Annika, Jucker, Mathias, Latz, Eicke, Wagner, Michael, Mengel, David, Synofzik, Matthis, Jessen, Frank, Ramirez, Alfredo, Ruiz, Agustín, and Heneka, Michael T.

Published
2022
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17. Left frontal hub connectivity delays cognitive impairment in autosomal-dominant and sporadic Alzheimer’s disease

Author

Franzmeier, Nicolai, Düzel, Emrah, Jessen, Frank, Buerger, Katharina, Levin, Johannes, Duering, Marco, Dichgans, Martin, Haass, Christian, Suárez-Calvet, Marc, Fagan, Anne M, Paumier, Katrina, Benzinger, Tammie, Masters, Colin L, Morris, John C, Perneczky, Robert, Janowitz, Daniel, Catak, Cihan, Wolfsgruber, Steffen, Wagner, Michael, Teipel, Stefan, Kilimann, Ingo, Ramirez, Alfredo, Rossor, Martin, Jucker, Mathias, Chhatwal, Jasmeer, Spottke, Annika, Boecker, Henning, Brosseron, Frederic, Falkai, Peter, Fliessbach, Klaus, Heneka, Michael T, Laske, Christoph, Nestor, Peter, Peters, Oliver, Fuentes, Manuel, Menne, Felix, Priller, Josef, Spruth, Eike J, Franke, Christiana, Schneider, Anja, Kofler, Barbara, Westerteicher, Christine, Speck, Oliver, Wiltfang, Jens, Bartels, Claudia, Caballero, Miguel Ángel Araque, Metzger, Coraline, Bittner, Daniel, Weiner, Michael, Lee, Jae-Hong, Salloway, Stephen, Danek, Adrian, Goate, Alison, Schofield, Peter R, Bateman, Randall J, and Ewers, Michael

Subjects
Clinical Trials and Supportive Activities, Brain Disorders, Aging, Basic Behavioral and Social Science, Dementia, Neurosciences, Behavioral and Social Science, Acquired Cognitive Impairment, Clinical Research, Alzheimer's Disease, Neurodegenerative, Biomedical Imaging, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aetiology, 2.1 Biological and endogenous factors, Neurological, Adult, Alzheimer Disease, Amyloid beta-Protein Precursor, Brain Mapping, Cognitive Dysfunction, Female, Frontal Lobe, Functional Laterality, Humans, Imaging, Three-Dimensional, Magnetic Resonance Imaging, Male, Middle Aged, Mutation, Nerve Net, Presenilin-1, Presenilin-2, Alzheimer's disease, cognitive reserve, resting state connectivity, memory, dementia biomarkers, Medical and Health Sciences, Psychology and Cognitive Sciences, Neurology & Neurosurgery
Abstract

Patients with Alzheimer's disease vary in their ability to sustain cognitive abilities in the presence of brain pathology. A major open question is which brain mechanisms may support higher reserve capacity, i.e. relatively high cognitive performance at a given level of Alzheimer's pathology. Higher functional MRI-assessed functional connectivity of a hub in the left frontal cortex is a core candidate brain mechanism underlying reserve as it is associated with education (i.e. a protective factor often associated with higher reserve) and attenuated cognitive impairment in prodromal Alzheimer's disease. However, no study has yet assessed whether such hub connectivity of the left frontal cortex supports reserve throughout the evolution of pathological brain changes in Alzheimer's disease, including the presymptomatic stage when cognitive decline is subtle. To address this research gap, we obtained cross-sectional resting state functional MRI in 74 participants with autosomal dominant Alzheimer's disease, 55 controls from the Dominantly Inherited Alzheimer's Network and 75 amyloid-positive elderly participants, as well as 41 amyloid-negative cognitively normal elderly subjects from the German Center of Neurodegenerative Diseases multicentre study on biomarkers in sporadic Alzheimer's disease. For each participant, global left frontal cortex connectivity was computed as the average resting state functional connectivity between the left frontal cortex (seed) and each voxel in the grey matter. As a marker of disease stage, we applied estimated years from symptom onset in autosomal dominantly inherited Alzheimer's disease and cerebrospinal fluid tau levels in sporadic Alzheimer's disease cases. In both autosomal dominant and sporadic Alzheimer's disease patients, higher levels of left frontal cortex connectivity were correlated with greater education. For autosomal dominant Alzheimer's disease, a significant left frontal cortex connectivity × estimated years of onset interaction was found, indicating slower decline of memory and global cognition at higher levels of connectivity. Similarly, in sporadic amyloid-positive elderly subjects, the effect of tau on cognition was attenuated at higher levels of left frontal cortex connectivity. Polynomial regression analysis showed that the trajectory of cognitive decline was shifted towards a later stage of Alzheimer's disease in patients with higher levels of left frontal cortex connectivity. Together, our findings suggest that higher resilience against the development of cognitive impairment throughout the early stages of Alzheimer's disease is at least partially attributable to higher left frontal cortex-hub connectivity.

Published
2018

23. INDUCED PLURIPOTENT STEM CELL-DERIVED MICROGLIA TO STUDY NLRP3 INFLAMMASOME ACTIVATION IN ALZHEIMER’S DISEASE.

Author

ÖNER, Aslı ERDOĞAN, DANSOKHO, Cira, KOISTINAHO, Jari, LEHTONEN, Sarka, SOLAKOĞLU, Seyhun, and HENEKA, Michael T.

Subjects
INDUCED pluripotent stem cells, PLURIPOTENT stem cells, ENZYME-linked immunosorbent assay, NLRP3 protein, PYRIN (Protein)
Abstract

Copyright of Journal of Istanbul Faculty of Medicine / İstanbul Tıp Fakültesi Dergisi is the property of Istanbul Tip Fakultesi Dergisi and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2024
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25. Aβ oligomers peak in early stages of Alzheimer's disease preceding tau pathology

Author

Blömeke, Lara, primary, Rehn, Fabian, additional, Kraemer‐Schulien, Victoria, additional, Kutzsche, Janine, additional, Pils, Marlene, additional, Bujnicki, Tuyen, additional, Lewczuk, Piotr, additional, Kornhuber, Johannes, additional, Freiesleben, Silka D., additional, Schneider, Luisa‐Sophie, additional, Preis, Lukas, additional, Priller, Josef, additional, Spruth, Eike J., additional, Altenstein, Slawek, additional, Lohse, Andrea, additional, Schneider, Anja, additional, Fliessbach, Klaus, additional, Wiltfang, Jens, additional, Hansen, Niels, additional, Rostamzadeh, Ayda, additional, Düzel, Emrah, additional, Glanz, Wenzel, additional, Incesoy, Enise I., additional, Butryn, Michaela, additional, Buerger, Katharina, additional, Janowitz, Daniel, additional, Ewers, Michael, additional, Perneczky, Robert, additional, Rauchmann, Boris‐Stephan, additional, Teipel, Stefan, additional, Kilimann, Ingo, additional, Goerss, Doreen, additional, Laske, Christoph, additional, Munk, Matthias H., additional, Sanzenbacher, Carolin, additional, Spottke, Annika, additional, Roy‐Kluth, Nina, additional, Heneka, Michael T., additional, Brosseron, Frederic, additional, Wagner, Michael, additional, Wolfsgruber, Steffen, additional, Kleineidam, Luca, additional, Stark, Melina, additional, Schmid, Matthias, additional, Jessen, Frank, additional, Bannach, Oliver, additional, Willbold, Dieter, additional, and Peters, Oliver, additional

Published
2024
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26. Silencing Apoe with divalent‐siRNAs improves amyloid burden and activates immune response pathways in Alzheimer's disease

Author

Ferguson, Chantal M., primary, Hildebrand, Samuel, additional, Godinho, Bruno M. D. C., additional, Buchwald, Julianna, additional, Echeverria, Dimas, additional, Coles, Andrew, additional, Grigorenko, Anastasia, additional, Vangjeli, Lorenc, additional, Sousa, Jacquelyn, additional, McHugh, Nicholas, additional, Hassler, Matthew, additional, Santarelli, Francesco, additional, Heneka, Michael T., additional, Rogaev, Evgeny, additional, and Khvorova, Anastasia, additional

Published
2024
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27. Multimodal MRI analysis of basal forebrain structure and function across the Alzheimer’s disease spectrum

Author

Herdick, Meret, Dyrba, Martin, Fritz, Hans-Christian J., Altenstein, Slawek, Ballarini, Tommaso, Brosseron, Frederic, Buerger, Katharina, Can Cetindag, Arda, Dechent, Peter, Dobisch, Laura, Duezel, Emrah, Ertl-Wagner, Birgit, Fliessbach, Klaus, Dawn Freiesleben, Silka, Frommann, Ingo, Glanz, Wenzel, Dylan Haynes, John, Heneka, Michael T., Janowitz, Daniel, Kilimann, Ingo, Laske, Christoph, Metzger, Coraline D., Munk, Matthias H., Peters, Oliver, Priller, Josef, Roy, Nina, Scheffler, Klaus, Schneider, Anja, Spottke, Annika, Jakob Spruth, Eike, Tscheuschler, Maike, Vukovich, Ruth, Wiltfang, Jens, Jessen, Frank, Teipel, Stefan, and Grothe, Michel J.

Published
2020
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29. Neuroinflammation in Alzheimer's disease

Author

Heneka, Michael T, Carson, Monica J, Khoury, Joseph El, Landreth, Gary E, Brosseron, Frederic, Feinstein, Douglas L, Jacobs, Andreas H, Wyss-Coray, Tony, Vitorica, Javier, Ransohoff, Richard M, Herrup, Karl, Frautschy, Sally A, Finsen, Bente, Brown, Guy C, Verkhratsky, Alexei, Yamanaka, Koji, Koistinaho, Jari, Latz, Eicke, Halle, Annett, Petzold, Gabor C, Town, Terrence, Morgan, Dave, Shinohara, Mari L, Perry, V Hugh, Holmes, Clive, Bazan, Nicolas G, Brooks, David J, Hunot, Stéphane, Joseph, Bertrand, Deigendesch, Nikolaus, Garaschuk, Olga, Boddeke, Erik, Dinarello, Charles A, Breitner, John C, Cole, Greg M, Golenbock, Douglas T, and Kummer, Markus P

Subjects
Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Neurosciences, Brain Disorders, Alzheimer's Disease, Acquired Cognitive Impairment, Prevention, Neurodegenerative, Dementia, Aging, Aetiology, 2.1 Biological and endogenous factors, Neurological, Inflammatory and immune system, Alzheimer Disease, Animals, Anti-Inflammatory Agents, Non-Steroidal, Astrocytes, Biomarkers, Brain Injuries, Clinical Trials as Topic, Disease Models, Animal, Disease Progression, Humans, Immunity, Innate, Immunization, Inflammation, Inflammation Mediators, Locus Coeruleus, Microglia, Nootropic Agents, Obesity, Phagocytosis, Protein Folding, Risk Factors, Severity of Illness Index, Clinical Sciences, Neurology & Neurosurgery
Abstract

Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and trigger an innate immune response characterised by release of inflammatory mediators, which contribute to disease progression and severity. Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease.

Published
2015

31. Common variants in Alzheimer’s disease and risk stratification by polygenic risk scores

Author

de Rojas, Itziar, Moreno-Grau, Sonia, Tesi, Niccolo, Grenier-Boley, Benjamin, Andrade, Victor, Jansen, Iris E., Pedersen, Nancy L., Stringa, Najada, Zettergren, Anna, Hernández, Isabel, Montrreal, Laura, Antúnez, Carmen, Antonell, Anna, Tankard, Rick M., Bis, Joshua C., Sims, Rebecca, Bellenguez, Céline, Quintela, Inés, González-Perez, Antonio, Calero, Miguel, Franco-Macías, Emilio, Macías, Juan, Blesa, Rafael, Cervera-Carles, Laura, Menéndez-González, Manuel, Frank-García, Ana, Royo, Jose Luís, Moreno, Fermin, Huerto Vilas, Raquel, Baquero, Miquel, Diez-Fairen, Mónica, Lage, Carmen, García-Madrona, Sebastián, García-González, Pablo, Alarcón-Martín, Emilio, Valero, Sergi, Sotolongo-Grau, Oscar, Ullgren, Abbe, Naj, Adam C., Lemstra, Afina W., Benaque, Alba, Pérez-Cordón, Alba, Benussi, Alberto, Rábano, Alberto, Padovani, Alessandro, Squassina, Alessio, de Mendonça, Alexandre, Arias Pastor, Alfonso, Kok, Almar A. L., Meggy, Alun, Pastor, Ana Belén, Espinosa, Ana, Corma-Gómez, Anaïs, Martín Montes, Angel, Sanabria, Ángela, DeStefano, Anita L., Schneider, Anja, Haapasalo, Annakaisa, Kinhult Ståhlbom, Anne, Tybjærg-Hansen, Anne, Hartmann, Annette M., Spottke, Annika, Corbatón-Anchuelo, Arturo, Rongve, Arvid, Borroni, Barbara, Arosio, Beatrice, Nacmias, Benedetta, Nordestgaard, Børge G., Kunkle, Brian W., Charbonnier, Camille, Abdelnour, Carla, Masullo, Carlo, Martínez Rodríguez, Carmen, Muñoz-Fernandez, Carmen, Dufouil, Carole, Graff, Caroline, Ferreira, Catarina B., Chillotti, Caterina, Reynolds, Chandra A., Fenoglio, Chiara, Van Broeckhoven, Christine, Clark, Christopher, Pisanu, Claudia, Satizabal, Claudia L., Holmes, Clive, Buiza-Rueda, Dolores, Aarsland, Dag, Rujescu, Dan, Alcolea, Daniel, Galimberti, Daniela, Wallon, David, Seripa, Davide, Grünblatt, Edna, Dardiotis, Efthimios, Düzel, Emrah, Scarpini, Elio, Conti, Elisa, Rubino, Elisa, Gelpi, Ellen, Rodriguez-Rodriguez, Eloy, Duron, Emmanuelle, Boerwinkle, Eric, Ferri, Evelyn, Tagliavini, Fabrizio, Küçükali, Fahri, Pasquier, Florence, Sanchez-Garcia, Florentino, Mangialasche, Francesca, Jessen, Frank, Nicolas, Gaël, Selbæk, Geir, Ortega, Gemma, Chêne, Geneviève, Hadjigeorgiou, Georgios, Rossi, Giacomina, Spalletta, Gianfranco, Giaccone, Giorgio, Grande, Giulia, Binetti, Giuliano, Papenberg, Goran, Hampel, Harald, Bailly, Henri, Zetterberg, Henrik, Soininen, Hilkka, Karlsson, Ida K., Alvarez, Ignacio, Appollonio, Ildebrando, Giegling, Ina, Skoog, Ingmar, Saltvedt, Ingvild, Rainero, Innocenzo, Rosas Allende, Irene, Hort, Jakub, Diehl-Schmid, Janine, Van Dongen, Jasper, Vidal, Jean-Sebastien, Lehtisalo, Jenni, Wiltfang, Jens, Thomassen, Jesper Qvist, Kornhuber, Johannes, Haines, Jonathan L., Vogelgsang, Jonathan, Pineda, Juan A., Fortea, Juan, Popp, Julius, Deckert, Jürgen, Buerger, Katharina, Morgan, Kevin, Fließbach, Klaus, Sleegers, Kristel, Molina-Porcel, Laura, Kilander, Lena, Weinhold, Leonie, Farrer, Lindsay A., Wang, Li-San, Kleineidam, Luca, Farotti, Lucia, Parnetti, Lucilla, Tremolizzo, Lucio, Hausner, Lucrezia, Benussi, Luisa, Froelich, Lutz, Ikram, M. Arfan, Deniz-Naranjo, M. Candida, Tsolaki, Magda, Rosende-Roca, Maitée, Löwenmark, Malin, Hulsman, Marc, Spallazzi, Marco, Pericak-Vance, Margaret A., Esiri, Margaret, Bernal Sánchez-Arjona, María, Dalmasso, Maria Carolina, Martínez-Larrad, María Teresa, Arcaro, Marina, Nöthen, Markus M., Fernández-Fuertes, Marta, Dichgans, Martin, Ingelsson, Martin, Herrmann, Martin J., Scherer, Martin, Vyhnalek, Martin, Kosmidis, Mary H., Yannakoulia, Mary, Schmid, Matthias, Ewers, Michael, Heneka, Michael T., Wagner, Michael, Scamosci, Michela, Kivipelto, Miia, Hiltunen, Mikko, Zulaica, Miren, Alegret, Montserrat, Fornage, Myriam, Roberto, Natalia, van Schoor, Natasja M., Seidu, Nazib M., Banaj, Nerisa, Armstrong, Nicola J., Scarmeas, Nikolaos, Scherbaum, Norbert, Goldhardt, Oliver, Hanon, Oliver, Peters, Oliver, Skrobot, Olivia Anna, Quenez, Olivier, Lerch, Ondrej, Bossù, Paola, Caffarra, Paolo, Dionigi Rossi, Paolo, Sakka, Paraskevi, Mecocci, Patrizia, Hoffmann, Per, Holmans, Peter A., Fischer, Peter, Riederer, Peter, Yang, Qiong, Marshall, Rachel, Kalaria, Rajesh N., Mayeux, Richard, Vandenberghe, Rik, Cecchetti, Roberta, Ghidoni, Roberta, Frikke-Schmidt, Ruth, Sorbi, Sandro, Hägg, Sara, Engelborghs, Sebastiaan, Helisalmi, Seppo, Botne Sando, Sigrid, Kern, Silke, Archetti, Silvana, Boschi, Silvia, Fostinelli, Silvia, Gil, Silvia, Mendoza, Silvia, Mead, Simon, Ciccone, Simona, Djurovic, Srdjan, Heilmann-Heimbach, Stefanie, Riedel-Heller, Steffi, Kuulasmaa, Teemu, del Ser, Teodoro, Lebouvier, Thibaud, Polak, Thomas, Ngandu, Tiia, Grimmer, Timo, Bessi, Valentina, Escott-Price, Valentina, Giedraitis, Vilmantas, Deramecourt, Vincent, Maier, Wolfgang, Jian, Xueqiu, Pijnenburg, Yolande A. L., Kehoe, Patrick Gavin, Garcia-Ribas, Guillermo, Sánchez-Juan, Pascual, Pastor, Pau, Pérez-Tur, Jordi, Piñol-Ripoll, Gerard, Lopez de Munain, Adolfo, García-Alberca, Jose María, Bullido, María J., Álvarez, Victoria, Lleó, Alberto, Real, Luis M., Mir, Pablo, Medina, Miguel, Scheltens, Philip, Holstege, Henne, Marquié, Marta, Sáez, María Eugenia, Carracedo, Ángel, Amouyel, Philippe, Schellenberg, Gerard D., Williams, Julie, Seshadri, Sudha, van Duijn, Cornelia M., Mather, Karen A., Sánchez-Valle, Raquel, Serrano-Ríos, Manuel, Orellana, Adelina, Tárraga, Lluís, Blennow, Kaj, Huisman, Martijn, Andreassen, Ole A., Posthuma, Danielle, Clarimón, Jordi, Boada, Mercè, van der Flier, Wiesje M., Ramirez, Alfredo, Lambert, Jean-Charles, van der Lee, Sven J., and Ruiz, Agustín

Published
2021
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34. A microRNA signature that correlates with cognition and is a target against cognitive decline

Author

Islam, Md Rezaul, Kaurani, Lalit, Berulava, Tea, Heilbronner, Urs, Budde, Monika, Centeno, Tonatiuh Pena, Elerdashvili, Vakthang, Zafieriou, Maria‐Patapia, Benito, Eva, Sertel, Sinem M, Goldberg, Maria, Senner, Fanny, Kalman, Janos L, Burkhardt, Susanne, Oepen, Anne Sophie, Sakib, Mohammad Sadman, Kerimoglu, Cemil, Wirths, Oliver, Bickeböller, Heike, Bartels, Claudia, Brosseron, Frederic, Buerger, Katharina, Cosma, Nicoleta‐Carmen, Fliessbach, Klaus, Heneka, Michael T., Janowitz, Daniel, Kilimann, Ingo, Kleinedam, Luca, Laske, Christoph, Metzger, Coraline D, Munk, Matthias H, Perneczky, Robert, Peters, Oliver, Priller, Josef, Rauchmann, Boris S., Roy, Nina, Schneider, Anja, Spottke, Annika, Spruth, Eike J, Teipel, Stefan, Tscheuschler, Maike, Wagner, Michael, Wiltfang, Jens, Düzel, Emrah, Jessen, Frank, Rizzoli, Silvio O, Zimmermann, Wolfram‐Hubertus, Schulze, Thomas G, Falkai, Peter, Sananbenesi, Farahnaz, and Fischer, Andre

Published
2021
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36. Inferior Frontal Sulcal Hyperintensities on Brain MRI Are Associated with Amyloid Positivity beyond Age—Results from the Multicentre Observational DELCODE Study.

Author

Dörner, Marc, Seebach, Katharina, Heneka, Michael T., Menze, Inga, von Känel, Roland, Euler, Sebastian, Schreiber, Frank, Arndt, Philipp, Neumann, Katja, Hildebrand, Annkatrin, John, Anna-Charlotte, Tyndall, Anthony, Kirchebner, Johannes, Tacik, Pawel, Jansen, Robin, Grimm, Alexander, Henneicke, Solveig, Perosa, Valentina, Meuth, Sven G., and Peters, Oliver

Subjects
AMYLOID, MAGNETIC resonance imaging, OPTIMISM, ALZHEIMER'S disease, MINI-Mental State Examination
Abstract

Inferior frontal sulcal hyperintensities (IFSHs) on fluid-attenuated inversion recovery (FLAIR) sequences have been proposed to be indicative of glymphatic dysfunction. Replication studies in large and diverse samples are nonetheless needed to confirm them as an imaging biomarker. We investigated whether IFSHs were tied to Alzheimer's disease (AD) pathology and cognitive performance. We used data from 361 participants along the AD continuum, who were enrolled in the multicentre DELCODE study. The IFSHs were rated visually based on FLAIR magnetic resonance imaging. We performed ordinal regression to examine the relationship between the IFSHs and cerebrospinal fluid-derived amyloid positivity and tau positivity (Aβ42/40 ratio ≤ 0.08; pTau181 ≥ 73.65 pg/mL) and linear regression to examine the relationship between cognitive performance (i.e., Mini-Mental State Examination and global cognitive and domain-specific performance) and the IFSHs. We controlled the models for age, sex, years of education, and history of hypertension. The IFSH scores were higher in those participants with amyloid positivity (OR: 1.95, 95% CI: 1.05–3.59) but not tau positivity (OR: 1.12, 95% CI: 0.57–2.18). The IFSH scores were higher in older participants (OR: 1.05, 95% CI: 1.00–1.10) and lower in males compared to females (OR: 0.44, 95% CI: 0.26–0.76). We did not find sufficient evidence linking the IFSH scores with cognitive performance after correcting for demographics and AD biomarker positivity. IFSHs may reflect the aberrant accumulation of amyloid β beyond age. [ABSTRACT FROM AUTHOR]

Published
2024
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40. NLRP3 inflammasome activation drives tau pathology

Author

Ising, Christina, Venegas, Carmen, Zhang, Shuangshuang, Scheiblich, Hannah, Schmidt, Susanne V., Vieira-Saecker, Ana, Schwartz, Stephanie, Albasset, Shadi, McManus, Róisín M., Tejera, Dario, Griep, Angelika, Santarelli, Francesco, Brosseron, Frederic, Opitz, Sabine, Stunden, James, Merten, Maximilian, Kayed, Rakez, Golenbock, Douglas T., Blum, David, Latz, Eicke, Buée, Luc, and Heneka, Michael T.

Published
2019
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44. In‐depth analysis of data from the RAS‐ALS study reveals new insights in rasagiline treatment for amyotrophic lateral sclerosis.

Author

Schuster, Joachim, Dreyhaupt, Jens, Mönkemöller, Karla, Dupuis, Luc, Dieterlé, Stéphane, Weishaupt, Jochen H., Kassubek, Jan, Petri, Susanne, Meyer, Thomas, Grosskreutz, Julian, Schrank, Berthold, Boentert, Matthias, Emmer, Alexander, Hermann, Andreas, Zeller, Daniel, Prudlo, Johannes, Winkler, Andrea S., Grehl, Torsten, Heneka, Michael T., and Johannesen, Siw

Subjects
AMYOTROPHIC lateral sclerosis, SINGLE nucleotide polymorphisms, DATA analysis, RANDOMIZED controlled trials, STATISTICAL power analysis
Abstract

Background and purpose: In 2016, we concluded a randomized controlled trial testing 1 mg rasagiline per day add‐on to standard therapy in 252 amyotrophic lateral sclerosis (ALS) patients. This article aims at better characterizing ALS patients who could possibly benefit from rasagiline by reporting new subgroup analysis and genetic data. Methods: We performed further exploratory in‐depth analyses of the study population and investigated the relevance of single nucleotide polymorphisms (SNPs) related to the dopaminergic system. Results: Placebo‐treated patients with very slow disease progression (loss of Amyotrophic Lateral Sclerosis Functional Rating Scale–Revised [ALSFRS‐R] per month before randomization of ≤0.328 points) showed a per se survival probability after 24 months of 0.85 (95% confidence interval = 0.65–0.94). The large group of intermediate to fast progressing ALS patients showed a prolonged survival in the rasagiline group compared to placebo after 6 and 12 months (p = 0.02, p = 0.04), and a reduced decline of ALSFRS‐R after 18 months (p = 0.049). SNP genotypes in the MAOB gene and DRD2 gene did not show clear associations with rasagiline treatment effects. Conclusions: These results underline the need to consider individual disease progression at baseline in future ALS studies. Very slow disease progressors compromise the statistical power of studies with treatment durations of 12–18 months using clinical endpoints. Analysis of MAOB and DRD2 SNPs revealed no clear relationship to any outcome parameter. More insights are expected from future studies elucidating whether patients with DRD2CC genotype (Rs2283265) show a pronounced benefit from treatment with rasagiline, pointing to the opportunities precision medicine could open up for ALS patients in the future. [ABSTRACT FROM AUTHOR]

Published
2024
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45. Microglia heterogeneity in health and disease.

Author

Dadwal, Shilauni and Heneka, Michael T.

Subjects
HOMEOSTASIS, MICROGLIA, HETEROGENEITY, IMMUNE response, NEURODEGENERATION
Abstract

Microglia, the resident immune cells of the central nervous system (CNS), have received significant attention due to their critical roles in maintaining brain homeostasis and mediating cerebral immune responses. Understanding the origin of microglia has been a subject of great interest, and emerging evidence suggests that microglia consist of multiple subpopulations with unique molecular and functional characteristics. These subpopulations of microglia may exhibit specialized roles in response to different environmental cues as in disease conditions. The newfound understanding of microglial heterogeneity has significant implications for elucidating their roles in both physiological and pathological conditions. In the context of disease, microglia have been studied rigorously as they play a very important role in neuroinflammation. Dysregulated microglial activation and function contribute to chronic inflammation. Further exploration of microglial heterogeneity and their interactions with other cell types in the CNS will undoubtedly pave the way to novel therapeutic strategies targeting microglia‐mediated pathologies. In this review, we discuss the latest advances in the field of microglia research, focusing specifically on the origin and subpopulations of microglia, the populations of microglia types in the brains of patients with neurodegenerative diseases, and how microglia are regulated in the healthy CNS. [ABSTRACT FROM AUTHOR]

Published
2024
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48. Corrigendum: mTOR-dependent translation amplifies microglia priming in aging mice

Author

Keane, Lily, Antignano, Ignazio, Riechers, Sean-Patrick, Zollinger, Raphael, Dumas, Anaelle A., Offermann, Nina, Bernis, Maria E., Russ, Jenny, Graelmann, Frederike, McCormick, Patrick Neil, Esser, Julia, Tejera, Dario, Nagano, Ai, Wang, Jun, Chelala, Claude, Biederbick, Yvonne, Halle, Annett, Salomoni, Paolo, Heneka, Michael T., and Capasso, Melania

Subjects
Health care industry
Abstract

Original citation: J Clin Invest. 2021;131(1):1-16. https://doi.org/10.1172/JCI132727. Citation for this corrigendum: J Clin Invest. 2021;131(20):e155208. https://doi.org/10.1172/JCI155208. During the preparation for this manuscript, the Western blots for p-4EBP1 Thr70 and p-4EBP1 [...]

Published
2021
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50. Brain Volume Changes after COVID-19 Compared to Healthy Controls by Artificial Intelligence-Based MRI Volumetry

Author

Bendella, Zeynep, primary, Widmann, Catherine Nichols, additional, Layer, Julian Philipp, additional, Layer, Yonah Lucas, additional, Haase, Robert, additional, Sauer, Malte, additional, Bieler, Luzie, additional, Lehnen, Nils Christian, additional, Paech, Daniel, additional, Heneka, Michael T., additional, Radbruch, Alexander, additional, and Schmeel, Frederic Carsten, additional

Published
2023
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