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2. 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

7. Early Inhibition of Phosphodiesterase 4B (PDE4B) Instills Cognitive Resilience in APPswe/PS1dE9 Mice

Author

Rombaut, Ben, primary, Schepers, Melissa, additional, Tiane, Assia, additional, Mussen, Femke, additional, Koole, Lisa, additional, Kessels, Sofie, additional, Trippaers, Chloë, additional, Jacobs, Ruben, additional, Wouters, Kristiaan, additional, Willems, Emily, additional, Veggel, Lieve van, additional, Koulousakis, Philippos, additional, Deluyker, Dorien, additional, Bito, Virginie, additional, Prickaerts, Jos, additional, Wens, Inez, additional, Brône, Bert, additional, van den Hove, Daniel L. A., additional, and Vanmierlo, Tim, additional

Published
2024
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10. CSF1R inhibition rescues tau pathology and neurodegeneration in an A/T/N model with combined AD pathologies, while preserving plaque associated microglia

Author

Lodder, Chritica, Scheyltjens, Isabelle, Stancu, Ilie Cosmin, Botella Lucena, Pablo, Gutiérrez de Ravé, Manuel, Vanherle, Sarah, Vanmierlo, Tim, Cremers, Niels, Vanrusselt, Hannah, Brône, Bert, Hanseeuw, Bernard, Octave, Jean-Noël, Bottelbergs, Astrid, Movahedi, Kiavash, and Dewachter, Ilse

Published
2021
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15. The effects of urolithin A on poly I:C-induced microglial activation.

Author

Mingo, Yakum Benard, Gabele, Lea, Lonnemann, Niklas, Brône, Bert, Korte, Martin, and Hosseini, Shirin

Subjects
MICROGLIA, ALZHEIMER'S disease, PARKINSON'S disease, VIRUS diseases, CYTOKINE release syndrome, CELL culture, VIRAL antibodies
Abstract

Neuroinflammation can be triggered by various stimuli, including viral infections. Viruses can directly invade the brain and infect neuronal cells or indirectly trigger a "cytokine storm" in the periphery that eventually leads to microglial activation in the brain. While this initial activation of microglial cells is important for viral clearance, chronic activation leads to excessive inflammation and oxidative stress, which can be neurotoxic. Remarkebly, recent studies have shown that certain viruses such as influenza A virus, coronavirus, herpes virus and Epstein-Barr virus may be involved in the development of neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, and multiple sclerosis. Therefore, it is important to find therapeutic strategies against chronic neuroinflammation triggered by viral infections. Here, we investigated the effects of urolithin A (UA) on microglial activation in vitro induced by a viral mimetic, poly I:C, in a triple co-culture system of neurons, astrocytes and microglial cells. Immunocytochemistry was used to perform a comprehensive singlecell analysis of the morphological changes of microglia as an indicator of their reactive state. Treatment with UA significantly prevented the poly I:C-induced reactive state of microglia, which was characterized by increased expression of the microglial activation markers CD68 and IBA-1. UA restored the poly I:Cinduced morphology by restoring microglial ramification. In addition, UA was able to reduce the release of the pro-inflammatory mediators CCL2, TNF-α, and IL-1β and showed a trend toward attenuation of cellular ROS production in poly I:C-treated cultures. Overall, this study suggests that UA as a component of a healthy diet may help prevent virus-induced neuroinflammation and may have therapeutic potential for future studies to prevent or treat neurodegenerative diseases by targeting the associated neuroinflammatory processes. [ABSTRACT FROM AUTHOR]

Published
2024
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20. Lack of the glycine receptor alpha 2 increases striatal activity and motivated behavior

Author

Devoght, Jens, primary, Comhair, Joris, additional, Morelli, Giovanni, additional, Rigo, Jean-Michel, additional, D’Hooge, Rudi, additional, Touma, Chadi, additional, Palme, Rupert, additional, Dewachter, Ilse, additional, vandeVen, Martin, additional, Harvey, Robert J., additional, Schiffmann, Serge, additional, Piccart, Elisabeth, additional, and Brône, Bert, additional

Published
2022
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24. Acute inhibition of transient receptor potential vanilloid‐type 4 cation channel halts cytoskeletal dynamism in microglia

Author

Beeken, Jolien, primary, Mertens, Melanie, additional, Stas, Nathan, additional, Kessels, Sofie, additional, Aerts, Liese, additional, Janssen, Bieke, additional, Mussen, Femke, additional, Pinto, Silvia, additional, Vennekens, Rudi, additional, Rigo, Jean‐Michel, additional, Nguyen, Laurent, additional, Brône, Bert, additional, and Alpizar, Yeranddy A., additional

Published
2022
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26. 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 J. L., 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, 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, Wyss-Coray, Tony, 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 J. L., 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, 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

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

27. Microglia states and nomenclature: A field at its crossroads.

Author

Paolicelli, Rosa RC, 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 BJL, Eyo, Ukpong, Galea, Elena, Garel, Sonia, Ginhoux, Florent, Glass, Christopher K, Gokce, Ozgun, Gomez-Nicola, Diego, González, Berta, Gordon, Siamon, Graeber, Manuel MB, Greenhalgh, Andrew AD, Gressens, Pierre, Greter, Melanie, Gutmann, David DH, Haass, Christian, Heneka, Michael MT, Heppner, Frank FL, Hong, Soyon, Hume, David DA, 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 JJ, Neniskyte, Urte, Neumann, Frank Harald, Noda, Mami, Peng, Bo, Peri, Francesca, Perry, Hugh VH, Popovich, Phillip PG, 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 WJ, Tay, Tuan Leng, Tsai, Li-Huei, Verkhratsky, Alexei, von Bernhardi, Rommy, Wake, Hiroaki, Wittamer, Valérie, Wolf, Susanne A, Wu, Long-Jun, Wyss-Coray, Tony, Paolicelli, Rosa RC, 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 BJL, Eyo, Ukpong, Galea, Elena, Garel, Sonia, Ginhoux, Florent, Glass, Christopher K, Gokce, Ozgun, Gomez-Nicola, Diego, González, Berta, Gordon, Siamon, Graeber, Manuel MB, Greenhalgh, Andrew AD, Gressens, Pierre, Greter, Melanie, Gutmann, David DH, Haass, Christian, Heneka, Michael MT, Heppner, Frank FL, Hong, Soyon, Hume, David DA, 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 JJ, Neniskyte, Urte, Neumann, Frank Harald, Noda, Mami, Peng, Bo, Peri, Francesca, Perry, Hugh VH, Popovich, Phillip PG, 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 WJ, 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

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., SCOPUS: re.j, info:eu-repo/semantics/published

Published
2022

30. Defining Microglial States and Nomenclature: A Roadmap to 2030

Author

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

Published
2022
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34. p27 kip1 Modulates the Morphology and Phagocytic Activity of Microglia.

Author

Beeken, Jolien, Kessels, Sofie, Rigo, Jean-Michel, Alpizar, Yeranddy A., Nguyen, Laurent, and Brône, Bert

Subjects
MICROGLIA, CELL migration, CELL cycle, MORPHOLOGY, BRAIN damage, PHAGOCYTOSIS, CEREBRAL cortex
Abstract

p27kip1 is a multifunctional protein that promotes cell cycle exit by blocking the activity of cyclin/cyclin-dependent kinase complexes as well as migration and motility via signaling pathways that converge on the actin and microtubule cytoskeleton. Despite the broad characterization of p27kip1 function in neural cells, little is known about its relevance in microglia. Here, we studied the role of p27kip1 in microglia using a combination of in vitro and in situ approaches. While the loss of p27kip1 did not affect microglial density in the cerebral cortex, it altered their morphological complexity in situ. However, despite the presence of p27kip1 in microglial processes, as shown by immunofluorescence in cultured cells, loss of p27kip1 did not change microglial process motility and extension after applying laser-induced brain damage in cortical brain slices. Primary microglia lacking p27kip1 showed increased phagocytic uptake of synaptosomes, while a cell cycle dead variant negatively affected phagocytosis. These findings indicate that p27kip1 plays specific roles in microglia. [ABSTRACT FROM AUTHOR]

Published
2022
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35. CSF1R inhibition rescues tau pathology and neurodegeneration in an A/T/N model with combined AD pathologies, while preserving plaque associated microglia.

Author

UCL - SSS/IONS/CEMO - Pôle Cellulaire et moléculaire, UCL - SSS/IONS/NEUR - Clinical Neuroscience, UCL - (SLuc) Service de neurologie, Lodder, Chritica, Scheyltjens, Isabelle, Stancu, Ilie Cosmin, Botella Lucena, Pablo, Gutiérrez de Ravé, Manuel, Vanherle, Sarah, Vanmierlo, Tim, Cremers, Niels, Vanrusselt, Hannah, Brône, Bert, Hanseeuw, Bernard, Octave, Jean-Noël, Bottelbergs, Astrid, Movahedi, Kiavash, Dewachter, Ilse, UCL - SSS/IONS/CEMO - Pôle Cellulaire et moléculaire, UCL - SSS/IONS/NEUR - Clinical Neuroscience, UCL - (SLuc) Service de neurologie, Lodder, Chritica, Scheyltjens, Isabelle, Stancu, Ilie Cosmin, Botella Lucena, Pablo, Gutiérrez de Ravé, Manuel, Vanherle, Sarah, Vanmierlo, Tim, Cremers, Niels, Vanrusselt, Hannah, Brône, Bert, Hanseeuw, Bernard, Octave, Jean-Noël, Bottelbergs, Astrid, Movahedi, Kiavash, and Dewachter, Ilse

Abstract

Alzheimer's disease (AD) is characterized by a sequential progression of amyloid plaques (A), neurofibrillary tangles (T) and neurodegeneration (N), constituting ATN pathology. While microglia are considered key contributors to AD pathogenesis, their contribution in the combined presence of ATN pathologies remains incompletely understood. As sensors of the brain microenvironment, microglial phenotypes and contributions are importantly defined by the pathologies in the brain, indicating the need for their analysis in preclinical models that recapitulate combined ATN pathologies, besides their role in A and T models only. Here, we report a new tau-seed model in which amyloid pathology facilitates bilateral tau propagation associated with brain atrophy, thereby recapitulating robust ATN pathology. Single-cell RNA sequencing revealed that ATN pathology exacerbated microglial activation towards disease-associated microglia states, with a significant upregulation of Apoe as compared to amyloid-only models (A). Importantly, Colony-Stimulating Factor 1 Receptor inhibition preferentially eliminated non-plaque-associated versus plaque associated microglia. The preferential depletion of non-plaque-associated microglia significantly attenuated tau pathology and neuronal atrophy, indicating their detrimental role during ATN progression. Together, our data reveal the intricacies of microglial activation and their contributions to pathology in a model that recapitulates the combined ATN pathologies of AD. Our data may provide a basis for microglia-targeting therapies selectively targeting detrimental microglial populations, while conserving protective populations.

Published
2021

36. The glycine receptor alpha 2 subunit in striatal development

Author

Schiffmann, Serge N., Rigo, Jean-Michel, Gall, David, Brône, Bert, Brion, Jean Pierre, Leroy, Karelle, Gubellini, Paolo, Aguayo, Luis, Lambrichts, Ivo, Comhair, Joris, Schiffmann, Serge N., Rigo, Jean-Michel, Gall, David, Brône, Bert, Brion, Jean Pierre, Leroy, Karelle, Gubellini, Paolo, Aguayo, Luis, Lambrichts, Ivo, and Comhair, Joris

Abstract

The work at hand will describe the influence of the Glycine receptor alpha 2 subunit and the glycinergic system on the development of Medium Spiny Neurons (MSNs) in the dorsal striatum. We will begin by giving a short introduction into the different structures of the CNS with deeper focus on the structures relevant for this work. Furthermore, we will introduce the neurons we investigate in this work and the different chapters. Finally, a more in depth introduction will describe the glycinergic system in the CNS and its most known physiological functions. Eventually we can establish the context in which we did this research about the effect of the Glycine receptor alpha 2 subunit in the development in medium spiny neurons (MSNs)., Doctorat en Sciences biomédicales et pharmaceutiques (Médecine), info:eu-repo/semantics/nonPublished

Published
2021

44. Microglial derived extracellular vesicles activate autophagy and mediate multi‐target signaling to maintain cellular homeostasis

Author

Van den Broek, Bram, primary, Pintelon, Isabel, additional, Hamad, Ibrahim, additional, Kessels, Sofie, additional, Haidar, Mansour, additional, Hellings, Niels, additional, Hendriks, Jerome J.A., additional, Kleinewietfeld, Markus, additional, Brône, Bert, additional, Timmerman, Vincent, additional, Timmermans, Jean‐Pierre, additional, Somers, Veerle, additional, Michiels, Luc, additional, and Irobi, Joy, additional

Published
2020
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48. MOESM1 of Chronic nigral neuromodulation aggravates behavioral deficits and synaptic changes in an α-synuclein based rat model for Parkinson’s disease

Author

Torre-Muruzabal, Teresa, Devoght, Jens, Haute, Chris Van Den, Brône, Bert, Perren, Anke Van Der, and Baekelandt, Veerle

Subjects
sense organs, eye diseases
Abstract

Additional file 1: Figure S1. Transduction efficiency of rAAV2/7 α-SYN and rAAV2/8 hM3Dq vector (tagged with mCherry tag) in DN. Figure S2. Chronic neuronal activity modulation in rAAV2/7 GFP vector injected animals does not affect motor behavior or TH+ cell numbers. Figure S3. Complete and uncropped western blots from Fig. 4. Figure S4. Complete and uncropped western blots from Fig. 5.

Published
2019
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50. Testosterone Induces Relaxation of Human Corpus Cavernosum Tissue of Patients With Erectile Dysfunction

Author

Van den Broeck, Thomas, primary, Soebadi, Mohammad Ayodhia, additional, Falter, Annelies, additional, Raets, Lore, additional, Duponselle, Jolien, additional, Lootsma, Joline, additional, Heintz, Alexander, additional, Philtjens, Uchelly, additional, Hofkens, Lien, additional, Gonzalez-Viedma, Arantxa, additional, Driesen, Karel, additional, Sandner, Peter, additional, Albersen, Maarten, additional, Brône, Bert, additional, and Van Renterghem, Koenraad, additional

Published
2019
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