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  1. AU=Weinhard Laetitia
  2. AU="Sun, Mi"
  3. AU="Pospísil, V"
  4. AU=Driscoll David R AU=Driscoll David R
  5. AU="Wojtalewicz, Nathalie"
  6. AU="Waingrow, Marshall"
  7. AU="Daymé Gonzalez Rodriguez"
  8. AU="Lou, Shuyi"
  9. AU="Figueiredo, Rodrigo S"
  10. AU=Fleet James C
  11. AU="Brohawn, David G"
  12. AU="Cho, Chun-Chieh"
  13. AU="van Raalte, Daniël H"
  14. AU="Zargarian, Loussiné"
  15. AU=Hascalovici Jacob
  16. AU="Spagnolo, Jennifer B"
  17. AU="Anderloni, Giulia"
  18. AU="Ahmad, Shoaib"
  19. AU="Du, Roujia"
  20. AU="Colmenero-Repiso, Ana"
  21. AU="Alvarez-Carbonell, David"
  22. AU="Phelippeau, Michael"
  23. AU="Lunghi, Laura"
  24. AU=Giersiepen Klaus
  25. AU="Drobyshev, Sergey"
  26. AU="Timme, Kathleen H"
  27. AU=Sfriso Paolo
  28. AU="Kim, John S"
  29. AU=Farkash Evan A AU=Farkash Evan A
  30. AU="Xia, Xueqian"

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  1. Artikel: Analysis of microglial BDNF function and expression in the motor cortex.

    Honey, Diana / Wosnitzka, Erin / Klann, Eric / Weinhard, Laetitia

    Frontiers in cellular neuroscience

    2022  Band 16, Seite(n) 961276

    Abstract: Brain-derived neurotrophic factor (BDNF) is a neurotrophin that regulates several aspects of brain function. Although numerous studies have demonstrated the expression and function of BDNF in neurons, its expression in microglia remains controversial. ... ...

    Abstract Brain-derived neurotrophic factor (BDNF) is a neurotrophin that regulates several aspects of brain function. Although numerous studies have demonstrated the expression and function of BDNF in neurons, its expression in microglia remains controversial. Using a combination of genetic tools and fluorescence imaging, we analyzed BDNF expression patterns and investigated the effect of microglial
    Sprache Englisch
    Erscheinungsdatum 2022-12-23
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2022.961276
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Headmasters

    Laetitia Weinhard / Paolo d'Errico / Tuan Leng Tay

    AIMS Molecular Science, Vol 5, Iss 1, Pp 63-

    Microglial regulation of learning and memory in health and disease

    2018  Band 89

    Abstract: Microglia are mononuclear phagocytes that reside throughout the lifetime of the animal in the central nervous system (CNS). Originating from the yolk sac, microglial progenitors infiltrate the developing brain anlage even before the formation of the ... ...

    Abstract Microglia are mononuclear phagocytes that reside throughout the lifetime of the animal in the central nervous system (CNS). Originating from the yolk sac, microglial progenitors infiltrate the developing brain anlage even before the formation of the neural network. Mature microglial cells persist by slow rates of self-renewal that vary across brain regions. Eminent studies in the recent decade have highlighted a role for steady state microglia in neurogenesis, synaptic pruning, and formation and maintenance of connectivity within the CNS, which are critical to learning and memory functions. Activity- and learning-dependent synaptic remodeling by microglia has been described in various contexts. Molecular pathways, including signaling through fractalkine CX3CL1 and its receptor CX3CR1, transforming growth factor-beta, classical complement system, colony-stimulating factor 1 receptor, adaptor protein DAP12, and brain-derived neurotropic factor, have been proposed to be important mediators of synaptic plasticity regulated by microglia. Reactive, dysfunctional, or aged microglia are thought to impact learning and memory, and are implicated in human neurodegenerative disorders in which dementia is a hallmark. These disorders include Nasu-Hakola disease, hereditary diffuse leukoencephaly with spheroids, Alzheimer’s disease, frontotemporal dementia, and Parkinson’s disease. Focusing on microglia, here we discuss the potential detrimental effects and risks presented by microglia-specific genetic variants, the environmental factors that target microglia, and microglial aging that likely lead to progressive memory loss in neurodegenerative diseases. Finally, we consider some caveats of the animal model systems that to date have advanced our understanding of microglial regulation of learning and memory.
    Schlagwörter microglia ; neurogenesis ; synaptic plasticity ; synaptic remodeling ; CX3CL1/CX3CR1 ; Alzheimer’s disease ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 612
    Sprache Englisch
    Erscheinungsdatum 2018-03-01T00:00:00Z
    Verlag AIMS Press
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Neuro-immune interactions in health and disease: Insights from FENS-Hertie 2022 Winter School.

    Binder, Luisa B / Rosa, Priscila B / de Sousa, Bárbara M / Chagas, Luana S / Dubljević, Olga / Martineau, Fanny Sandrine / Mottarlini, Francesca / Castany, Sílvia / Morton, Lorena / Krstanović, Fran / Tassinari, Isadora D / Choconta, Jeiny L / Pereira-Santos, Ana Raquel / Weinhard, Laetitia / Pallegar, Praveen N / Vahsen, Björn F / Lepiarz-Raba, Izabela / Compagnion, Anne-Claire / Lorente-Picón, Marina

    The European journal of neuroscience

    2024  Band 59, Heft 8, Seite(n) 1977–1992

    Abstract: In a great partnership, the Federation of European Neuroscience Societies (FENS) and the Hertie Foundation organized the FENS-Hertie 2022 Winter School on 'Neuro-immune interactions in health and disease'. The school selected 27 PhD students and 13 ... ...

    Abstract In a great partnership, the Federation of European Neuroscience Societies (FENS) and the Hertie Foundation organized the FENS-Hertie 2022 Winter School on 'Neuro-immune interactions in health and disease'. The school selected 27 PhD students and 13 postdoctoral fellows from 20 countries and involved 14 faculty members experts in the field. The Winter School focused on a rising field of research, the interactions between the nervous and both innate and adaptive immune systems under pathological and physiological conditions. A fine-tuned neuro-immune crosstalk is fundamental for healthy development, while disrupted neuro-immune communication might play a role in neurodegeneration, neuroinflammation and aging. However, much is yet to be understood about the underlying mechanisms of these neuro-immune interactions in the healthy brain and under pathological scenarios. In addition to new findings in this emerging field, novel methodologies and animal models were presented to foment research on neuro-immunology. The FENS-Hertie 2022 Winter School provided an insightful knowledge exchange between students and faculty focusing on the latest discoveries in the biology of neuro-immune interactions while fostering great academic and professional opportunities for early-career neuroscientists from around the world.
    Mesh-Begriff(e) Animals ; Humans ; Neuroimmunomodulation ; Neurosciences ; Brain ; Schools ; Aging
    Sprache Englisch
    Erscheinungsdatum 2024-02-04
    Erscheinungsland France
    Dokumenttyp Editorial
    ZDB-ID 645180-9
    ISSN 1460-9568 ; 0953-816X
    ISSN (online) 1460-9568
    ISSN 0953-816X
    DOI 10.1111/ejn.16262
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  4. Artikel ; Online: Microglia complement signaling promotes neuronal elimination and normal brain functional connectivity.

    Deivasigamani, Senthilkumar / Miteva, Mariya T / Natale, Silvia / Gutierrez-Barragan, Daniel / Basilico, Bernadette / Di Angelantonio, Silvia / Weinhard, Laetitia / Molotkov, Dmitry / Deb, Sukrita / Pape, Constantin / Bolasco, Giulia / Galbusera, Alberto / Asari, Hiroki / Gozzi, Alessandro / Ragozzino, Davide / Gross, Cornelius T

    Cerebral cortex (New York, N.Y. : 1991)

    2023  Band 33, Heft 21, Seite(n) 10750–10760

    Abstract: Complement signaling is thought to serve as an opsonization signal to promote the phagocytosis of synapses by microglia. However, while its role in synaptic remodeling has been demonstrated in the retino-thalamic system, it remains unclear whether ... ...

    Abstract Complement signaling is thought to serve as an opsonization signal to promote the phagocytosis of synapses by microglia. However, while its role in synaptic remodeling has been demonstrated in the retino-thalamic system, it remains unclear whether complement signaling mediates synaptic pruning in the brain more generally. Here we found that mice lacking the Complement receptor 3, the major microglia complement receptor, failed to show a deficit in either synaptic pruning or axon elimination in the developing mouse cortex. Instead, mice lacking Complement receptor 3 exhibited a deficit in the perinatal elimination of neurons in the cortex, a deficit that is associated with increased cortical thickness and enhanced functional connectivity in these regions in adulthood. These data demonstrate a role for complement in promoting neuronal elimination in the developing cortex.
    Mesh-Begriff(e) Mice ; Animals ; Microglia ; Neurons ; Brain ; Signal Transduction ; Synapses/physiology ; Receptors, Complement ; Neuronal Plasticity/physiology
    Chemische Substanzen Receptors, Complement
    Sprache Englisch
    Erscheinungsdatum 2023-09-16
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1077450-6
    ISSN 1460-2199 ; 1047-3211
    ISSN (online) 1460-2199
    ISSN 1047-3211
    DOI 10.1093/cercor/bhad313
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel: Three-Dimensional Nanostructure of an Intact Microglia Cell.

    Bolasco, Giulia / Weinhard, Laetitia / Boissonnet, Tom / Neujahr, Ralph / Gross, Cornelius T

    Frontiers in neuroanatomy

    2018  Band 12, Seite(n) 105

    Sprache Englisch
    Erscheinungsdatum 2018-12-05
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2452969-2
    ISSN 1662-5129
    ISSN 1662-5129
    DOI 10.3389/fnana.2018.00105
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  6. Artikel ; Online: Sexual dimorphism of microglia and synapses during mouse postnatal development.

    Weinhard, Laetitia / Neniskyte, Urte / Vadisiute, Auguste / di Bartolomei, Giulia / Aygün, Nil / Riviere, Laurie / Zonfrillo, Francesca / Dymecki, Susan / Gross, Cornelius

    Developmental neurobiology

    2018  Band 78, Heft 6, Seite(n) 618–626

    Abstract: Microglia participate in synapse remodeling in the cortex and hippocampus during mouse postnatal development. Although sex differences in microglia activity during embryonic development have been reported in these regions, it remains unexplored whether ... ...

    Abstract Microglia participate in synapse remodeling in the cortex and hippocampus during mouse postnatal development. Although sex differences in microglia activity during embryonic development have been reported in these regions, it remains unexplored whether microglia show sexually dimorphic features during the early postnatal period, a critical window for synapse formation and maturation. Here, we investigated morphological and functional features of microglia across early postnatal development as well as morphological features of both pre- and postsynaptic neuronal compartments in the mouse hippocampus. We found a sex-dependent shift in microglia volume and phagocytic capacity across the first four postnatal weeks. Measurements of synaptic features revealed sex differences in the density of synaptic spines and boutons during the second postnatal week. These data are consistent with a precocious development of both microglia and synapses in the female brain. We further hypothesize that this bias may contribute to sex-specific brain wiring. © 2017 The Authors. Developmental Neurobiology Published by Wiley Periodicals, Inc. Develop Neurobiol 78: 618-626, 2018.
    Mesh-Begriff(e) Animals ; Dendritic Spines/physiology ; Female ; Hippocampus/cytology ; Hippocampus/growth & development ; Hippocampus/physiology ; Male ; Mice, Inbred C57BL ; Mice, Transgenic ; Microglia/cytology ; Microglia/physiology ; Phagocytosis/physiology ; Sex Characteristics ; Synapses/physiology
    Sprache Englisch
    Erscheinungsdatum 2018-01-04
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2256184-5
    ISSN 1932-846X ; 1097-4695 ; 1932-8451 ; 0022-3034
    ISSN (online) 1932-846X ; 1097-4695
    ISSN 1932-8451 ; 0022-3034
    DOI 10.1002/dneu.22568
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  7. Artikel ; Online: Microglia remodel synapses by presynaptic trogocytosis and spine head filopodia induction.

    Weinhard, Laetitia / di Bartolomei, Giulia / Bolasco, Giulia / Machado, Pedro / Schieber, Nicole L / Neniskyte, Urte / Exiga, Melanie / Vadisiute, Auguste / Raggioli, Angelo / Schertel, Andreas / Schwab, Yannick / Gross, Cornelius T

    Nature communications

    2018  Band 9, Heft 1, Seite(n) 1228

    Abstract: Microglia are highly motile glial cells that are proposed to mediate synaptic pruning during neuronal circuit formation. Disruption of signaling between microglia and neurons leads to an excess of immature synaptic connections, thought to be the result ... ...

    Abstract Microglia are highly motile glial cells that are proposed to mediate synaptic pruning during neuronal circuit formation. Disruption of signaling between microglia and neurons leads to an excess of immature synaptic connections, thought to be the result of impaired phagocytosis of synapses by microglia. However, until now the direct phagocytosis of synapses by microglia has not been reported and fundamental questions remain about the precise synaptic structures and phagocytic mechanisms involved. Here we used light sheet fluorescence microscopy to follow microglia-synapse interactions in developing organotypic hippocampal cultures, complemented by a 3D ultrastructural characterization using correlative light and electron microscopy (CLEM). Our findings define a set of dynamic microglia-synapse interactions, including the selective partial phagocytosis, or trogocytosis (trogo-: nibble), of presynaptic structures and the induction of postsynaptic spine head filopodia by microglia. These findings allow us to propose a mechanism for the facilitatory role of microglia in synaptic circuit remodeling and maturation.
    Mesh-Begriff(e) Animals ; Hippocampus/physiology ; Macrophage-1 Antigen/metabolism ; Mice, Inbred C57BL ; Mice, Transgenic ; Microglia/physiology ; Models, Biological ; Neuronal Plasticity ; Phagocytosis ; Presynaptic Terminals/physiology ; Pseudopodia/physiology ; Signal Transduction ; Synapses/physiology
    Chemische Substanzen Macrophage-1 Antigen
    Sprache Englisch
    Erscheinungsdatum 2018-03-26
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-018-03566-5
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  8. Artikel ; Online: Microglia shape presynaptic properties at developing glutamatergic synapses.

    Basilico, Bernadette / Pagani, Francesca / Grimaldi, Alfonso / Cortese, Barbara / Di Angelantonio, Silvia / Weinhard, Laetitia / Gross, Cornelius / Limatola, Cristina / Maggi, Laura / Ragozzino, Davide

    Glia

    2018  Band 67, Heft 1, Seite(n) 53–67

    Abstract: Deficient neuron-microglia signaling during brain development is associated with abnormal synaptic maturation. However, the precise impact of deficient microglia function on synaptic maturation and the mechanisms involved remain poorly defined. Here we ... ...

    Abstract Deficient neuron-microglia signaling during brain development is associated with abnormal synaptic maturation. However, the precise impact of deficient microglia function on synaptic maturation and the mechanisms involved remain poorly defined. Here we report that mice defective in neuron-to-microglia signaling via the fractalkine receptor (Cx3cr1 KO) show reduced microglial branching and altered motility and develop widespread deficits in glutamatergic neurotransmission. We characterized the functional properties of CA3-CA1 synapses in hippocampal slices from these mice and found that they display altered glutamatergic release probability, maintaining immature properties also at late developmental stages. In particular, CA1 synapses of Cx3cr1 KO show (i) immature AMPA/NMDA ratio across developmental time, displaying a normal NMDA component and a defective AMPA component of EPSC; (ii) defective functional connectivity, as demonstrated by reduced current amplitudes in the input/output curve; and (iii) greater facilitation in the paired pulse ratio (PPR), suggesting decreased release probability. In addition, minimal stimulation experiments revealed that excitatory synapses have normal potency, but an increased number of failures, confirming a deficit in presynaptic release. Consistently, KO mice were characterized by higher number of silent synapses in comparison to WT. The presynaptic deficits were corrected by performing experiments in conditions of high release probability (Ca
    Mesh-Begriff(e) Animals ; Excitatory Postsynaptic Potentials ; Glutamic Acid/physiology ; Hippocampus/cytology ; Hippocampus/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microglia/physiology ; Neurons/physiology ; Organ Culture Techniques ; Presynaptic Terminals/physiology ; Synapses/physiology
    Chemische Substanzen Glutamic Acid (3KX376GY7L)
    Sprache Englisch
    Erscheinungsdatum 2018-11-11
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639414-0
    ISSN 1098-1136 ; 0894-1491
    ISSN (online) 1098-1136
    ISSN 0894-1491
    DOI 10.1002/glia.23508
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  9. Artikel ; Online: Microglia remodel synapses by presynaptic trogocytosis and spine head filopodia induction

    Laetitia Weinhard / Giulia di Bartolomei / Giulia Bolasco / Pedro Machado / Nicole L. Schieber / Urte Neniskyte / Melanie Exiga / Auguste Vadisiute / Angelo Raggioli / Andreas Schertel / Yannick Schwab / Cornelius T. Gross

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Band 14

    Abstract: Direct visualization of microglia-mediated synapse pruning has been lacking. This study shows direct evidence of microglia-synapse interaction where microglia do not necessarily ‘eat’ post-synaptic structure but ‘nibble’ on pre-synaptic terminals, much ... ...

    Abstract Direct visualization of microglia-mediated synapse pruning has been lacking. This study shows direct evidence of microglia-synapse interaction where microglia do not necessarily ‘eat’ post-synaptic structure but ‘nibble’ on pre-synaptic terminals, much akin to trogocytosis by lymphocytes.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2018-03-01T00:00:00Z
    Verlag Nature Publishing Group
    Dokumenttyp Artikel ; Online
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  10. Artikel ; Online: Microglia remodel synapses by presynaptic trogocytosis and spine head filopodia induction

    Laetitia Weinhard / Giulia di Bartolomei / Giulia Bolasco / Pedro Machado / Nicole L. Schieber / Urte Neniskyte / Melanie Exiga / Auguste Vadisiute / Angelo Raggioli / Andreas Schertel / Yannick Schwab / Cornelius T. Gross

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Band 14

    Abstract: Direct visualization of microglia-mediated synapse pruning has been lacking. This study shows direct evidence of microglia-synapse interaction where microglia do not necessarily ‘eat’ post-synaptic structure but ‘nibble’ on pre-synaptic terminals, much ... ...

    Abstract Direct visualization of microglia-mediated synapse pruning has been lacking. This study shows direct evidence of microglia-synapse interaction where microglia do not necessarily ‘eat’ post-synaptic structure but ‘nibble’ on pre-synaptic terminals, much akin to trogocytosis by lymphocytes.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2018-03-01T00:00:00Z
    Verlag Nature Portfolio
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