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  1. Article ; Online: Social isolation produces a sex- and brain region-specific alteration of microglia state.

    Vu, Alex P / Lam, David / Denney, Cayla / Lee, Kelly V / Plemel, Jason R / Jackson, Jesse

    The European journal of neuroscience

    2023  Volume 57, Issue 9, Page(s) 1481–1497

    Abstract: Social isolation is a profound form of psychological stress that impacts the mental health of a large proportion of society. Other experimental models of stress have demonstrated a microglia response that serves either a protective or pathological ... ...

    Abstract Social isolation is a profound form of psychological stress that impacts the mental health of a large proportion of society. Other experimental models of stress have demonstrated a microglia response that serves either a protective or pathological function. However, the effect of adult social isolation on microglia has not been thoroughly investigated. We measured microglia territory, branching, end points and phagocytic-lysosomal activity in group housed C57Bl/6 mice and mice that were socially isolated for 2 weeks. Our results show that the dorsomedial hypothalamus and hippocampal CA2 region of adult male mice undergo increased microglia volume, territory and endpoints following social isolation, whereas females exhibit this increase in the hypothalamus only. Males exhibited decreases in the phagocytic-lysosomal marker CD68 in microglia in these regions, whereas females showed an increase in CD68 in the hypothalamus suggesting sexually dimorphic and brain region-specific change in microglia state in response to social isolation. The prefrontal cortex, central amygdala, nucleus accumbens shell and visual cortex did not exhibit changes in microglia structure in either male or female mice. These data show that microglia in different brain regions undergo a distinct response to social isolation which may account for changes in cognition and behaviour associated with this prevalent form of psychological stress.
    MeSH term(s) Mice ; Male ; Female ; Animals ; Microglia/pathology ; Brain ; Social Isolation ; Hypothalamus ; Prefrontal Cortex
    Language English
    Publishing date 2023-03-23
    Publishing country France
    Document type Journal Article
    ZDB-ID 645180-9
    ISSN 1460-9568 ; 0953-816X
    ISSN (online) 1460-9568
    ISSN 0953-816X
    DOI 10.1111/ejn.15966
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Microglia promote remyelination independent of their role in clearing myelin debris.

    Baaklini, Charbel S / Ho, Madelene F S / Lange, Tristan / Hammond, Brady P / Panda, Sharmistha P / Zirngibl, Martin / Zia, Sameera / Himmelsbach, Kassandre / Rana, Heli / Phillips, Braxton / Antoszko, Daria / Ibanga, Jeremies / Lopez, Mizuki / Lee, Kelly V / Keough, Michael B / Caprariello, Andrew V / Kerr, Bradley J / Plemel, Jason R

    Cell reports

    2023  Volume 42, Issue 12, Page(s) 113574

    Abstract: Multiple sclerosis (MS) is an inflammatory disease characterized by myelin loss. While therapies exist to slow MS progression, no treatment currently exists for remyelination. Remyelination, linked to reduced disability in MS, relies on microglia and ... ...

    Abstract Multiple sclerosis (MS) is an inflammatory disease characterized by myelin loss. While therapies exist to slow MS progression, no treatment currently exists for remyelination. Remyelination, linked to reduced disability in MS, relies on microglia and monocyte-derived macrophages (MDMs). This study aims to understand the role of microglia during remyelination by lineage tracing and depleting them. Microglial lineage tracing reveals that both microglia and MDMs initially accumulate, but microglia later dominate the lesion. Microglia and MDMs engulf equal amounts of inhibitory myelin debris, but after microglial depletion, MDMs compensate by engulfing more myelin debris. Microglial depletion does, however, reduce the recruitment and proliferation of oligodendrocyte progenitor cells (OPCs) and impairs their subsequent differentiation and remyelination. These findings underscore the essential role of microglia during remyelination and offer insights for enhancing this process by understanding microglial regulation of remyelination.
    MeSH term(s) Humans ; Myelin Sheath/pathology ; Microglia/pathology ; Remyelination ; Demyelinating Diseases/pathology ; Macrophages/pathology ; Multiple Sclerosis/pathology
    Language English
    Publishing date 2023-12-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2023.113574
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Single-cell microglial transcriptomics during demyelination defines a microglial state required for lytic carcass clearance.

    Zia, Sameera / Hammond, Brady P / Zirngibl, Martin / Sizov, Anastasia / Baaklini, Charbel S / Panda, Sharmistha P / Ho, Madelene F S / Lee, Kelly V / Mainali, Apurba / Burr, Mena K / Williams, Sioned / Caprariello, Andrew V / Power, Christopher / Simmen, Thomas / Kerr, Bradley J / Plemel, Jason R

    Molecular neurodegeneration

    2022  Volume 17, Issue 1, Page(s) 82

    Abstract: Background: Microglia regulate the response to injury and disease in the brain and spinal cord. In white matter diseases microglia may cause demyelination. However, how microglia respond and regulate demyelination is not fully understood.: Methods: ... ...

    Abstract Background: Microglia regulate the response to injury and disease in the brain and spinal cord. In white matter diseases microglia may cause demyelination. However, how microglia respond and regulate demyelination is not fully understood.
    Methods: To understand how microglia respond during demyelination, we fed mice cuprizone-a potent demyelinating agent-and assessed the dynamics of genetically fate-mapped microglia. We then used single-cell RNA sequencing to identify and track the microglial subpopulations that arise during demyelination. To understand how microglia contribute to the clearance of dead oligodendrocytes, we ablated microglia starting at the peak of cuprizone-induced cell death and used the viability dye acridine orange to monitor apoptotic and lytic cell morphologies after microglial ablation. Lastly, we treated serum-free primary microglial cultures to model distinct aspects of cuprizone-induced demyelination and assessed the response.
    Results: The cuprizone diet generated a robust microglial response by week 4 of the diet. Single-cell RNA sequencing at this time point revealed the presence of several cuprizone-associated microglia (CAM) clusters. These clusters expressed a transcriptomic signature indicative of cytokine regulation and reactive oxygen species production with altered lysosomal and metabolic changes consistent with ongoing phagocytosis. Using acridine orange to monitor apoptotic and lytic cell death after microglial ablation, we found that microglia preferentially phagocytose lytic carcasses. In culture, microglia exposed to lytic carcasses partially recapitulated the CAM state, suggesting that phagocytosis contributes to this distinct microglial state during cuprizone demyelination.
    Conclusions: Microglia serve multiple roles during demyelination, yet their transcriptomic state resembles other neurodegenerative conditions. The phagocytosis of cellular debris is likely a universal cause for a common neurodegenerative microglial state.
    MeSH term(s) Animals ; Mice ; Cuprizone/toxicity ; Cuprizone/metabolism ; Microglia/metabolism ; Demyelinating Diseases/chemically induced ; Demyelinating Diseases/metabolism ; Transcriptome ; Acridine Orange/adverse effects ; Acridine Orange/metabolism ; Mice, Inbred C57BL ; Disease Models, Animal
    Chemical Substances Cuprizone (5N16U7E0AO) ; Acridine Orange (F30N4O6XVV)
    Language English
    Publishing date 2022-12-13
    Publishing country England
    Document type Journal Article
    ZDB-ID 2244557-2
    ISSN 1750-1326 ; 1750-1326
    ISSN (online) 1750-1326
    ISSN 1750-1326
    DOI 10.1186/s13024-022-00584-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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