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Article: Clusterin/apolipoprotein J, its isoforms and Alzheimer's disease.

Milinkeviciute, Giedre / Green, Kim N

2023 Volume 15, Page(s) 1167886

Language	English
Publishing date	2023-04-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2023.1167886
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Article ; Online: On the utility of CSF1R inhibitors.

Green, Kim N / Hume, David A

Proceedings of the National Academy of Sciences of the United States of America

2021 Volume 118, Issue 4

MeSH term(s)	Hematopoiesis ; Macrophages ; Receptor Protein-Tyrosine Kinases ; Receptors, Colony-Stimulating Factor
Chemical Substances	Receptors, Colony-Stimulating Factor ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2021-01-14
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2019695118
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Article ; Online: Selective targeting and modulation of plaque associated microglia via systemic hydroxyl dendrimer administration in an Alzheimer's disease mouse model.

Henningfield, Caden M / Soni, Neelakshi / Lee, Ryan W / Sharma, Rishi / Cleland, Jeffrey L / Green, Kim N

Alzheimer's research & therapy

2024 Volume 16, Issue 1, Page(s) 101

Abstract: Background: In Alzheimer's disease (AD), microglia surround extracellular plaques and mount a sustained inflammatory response, contributing to the pathogenesis of the disease. Identifying approaches to specifically target plaque-associated microglia ( ... ...

Abstract	Background: In Alzheimer's disease (AD), microglia surround extracellular plaques and mount a sustained inflammatory response, contributing to the pathogenesis of the disease. Identifying approaches to specifically target plaque-associated microglia (PAMs) without interfering in the homeostatic functions of non-plaque associated microglia would afford a powerful tool and potential therapeutic avenue. Methods: Here, we demonstrated that a systemically administered nanomedicine, hydroxyl dendrimers (HDs), can cross the blood brain barrier and are preferentially taken up by PAMs in a mouse model of AD. As proof of principle, to demonstrate biological effects in PAM function, we treated the 5xFAD mouse model of amyloidosis for 4 weeks via systemic administration (ip, 2x weekly) of HDs conjugated to a colony stimulating factor-1 receptor (CSF1R) inhibitor (D-45113). Results: Treatment resulted in significant reductions in amyloid-beta (Aβ) and a stark reduction in the number of microglia and microglia-plaque association in the subiculum and somatosensory cortex, as well as a downregulation in microglial, inflammatory, and synaptic gene expression compared to vehicle treated 5xFAD mice. Conclusions: This study demonstrates that systemic administration of a dendranib may be utilized to target and modulate PAMs.
MeSH term(s)	Animals ; Alzheimer Disease/drug therapy ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Microglia/drug effects ; Microglia/metabolism ; Dendrimers ; Plaque, Amyloid/drug therapy ; Plaque, Amyloid/pathology ; Mice, Transgenic ; Disease Models, Animal ; Mice ; Amyloid beta-Peptides/metabolism ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/antagonists & inhibitors ; Humans
Chemical Substances	Dendrimers ; Amyloid beta-Peptides ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor ; Csf1r protein, mouse
Language	English
Publishing date	2024-05-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2506521-X
ISSN	1758-9193 ; 1758-9193
ISSN (online)	1758-9193
ISSN	1758-9193
DOI	10.1186/s13195-024-01470-3
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Article: Microglia influence immune responses and restrict neurologic disease in response to central nervous system infection by a neurotropic murine coronavirus.

Syage, Amber / Pachow, Collin / Cheng, Yuting / Mangale, Vrushali / Green, Kim N / Lane, Thomas E

Frontiers in cellular neuroscience

2023 Volume 17, Page(s) 1291255

Abstract: Intracranial (i.c.) inoculation of susceptible mice with a glial-tropic strain of mouse hepatitis virus (JHMV), a murine coronavirus, results in an acute encephalomyelitis followed by viral persistence in white matter tracts accompanied by chronic ... ...

Abstract	Intracranial (i.c.) inoculation of susceptible mice with a glial-tropic strain of mouse hepatitis virus (JHMV), a murine coronavirus, results in an acute encephalomyelitis followed by viral persistence in white matter tracts accompanied by chronic neuroinflammation and demyelination. Microglia serve numerous functions including maintenance of the healthy central nervous system (CNS) and are among the first responders to injury or infection. More recently, studies have demonstrated that microglia aid in tailoring innate and adaptive immune responses following infection by neurotropic viruses including flaviviruses, herpesviruses, and picornaviruses. These findings have emphasized an important role for microglia in host defense against these viral pathogens. In addition, microglia are also critical in optimizing immune-mediated control of JHMV replication within the CNS while restricting the severity of demyelination and enhancing remyelination. This review will highlight our current understanding of the molecular and cellular mechanisms by which microglia aid in host defense, limit neurologic disease, and promote repair following CNS infection by a neurotropic murine coronavirus.
Language	English
Publishing date	2023-11-30
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2023.1291255
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Article ; Online: Commentary: How Do Microglia Regulate Neural Circuit Connectivity and Activity in the Adult Brain?

Liu, Yong-Jun / Green, Kim N / Holmes, Todd C / Xu, Xiangmin

Neuroscience insights

2022 Volume 17, Page(s) 26331055211071124

Abstract: Microglia are the primary immune cells in CNS. Recent work shows that microglia are also essential for proper brain development through synaptic pruning and remodeling during early life development. But the question of whether and how microglia regulate ... ...

Abstract	Microglia are the primary immune cells in CNS. Recent work shows that microglia are also essential for proper brain development through synaptic pruning and remodeling during early life development. But the question of whether and how microglia regulate synaptic connectivity in the adult brain remains open. Our recently published study provides new insights into the functional roles of microglia in the adult mouse brain. We find that chronic depletion of microglia via CSF1R inhibitors in the visual cortex in adult mice induces a dramatic increase in perineuronal nets, and enhances neural activities of both excitatory neurons and parvalbumin interneurons. These findings highlight new potential therapeutic avenues to enhance adult neural plasticity by manipulating microglia.
Language	English
Publishing date	2022-01-24
Publishing country	United States
Document type	Journal Article ; Comment
ISSN	2633-1055
ISSN (online)	2633-1055
DOI	10.1177/26331055211071124
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Article ; Online: Cortical diurnal rhythms remain intact with microglial depletion.

Barahona, Rocio A / Morabito, Samuel / Swarup, Vivek / Green, Kim N

Scientific reports

2022 Volume 12, Issue 1, Page(s) 114

Abstract: Microglia are subject to change in tandem with the endogenously generated biological oscillations known as our circadian rhythm. Studies have shown microglia harbor an intrinsic molecular clock which regulates diurnal changes in morphology and influences ...

Abstract	Microglia are subject to change in tandem with the endogenously generated biological oscillations known as our circadian rhythm. Studies have shown microglia harbor an intrinsic molecular clock which regulates diurnal changes in morphology and influences inflammatory responses. In the adult brain, microglia play an important role in the regulation of condensed extracellular matrix structures called perineuronal nets (PNNs), and it has been suggested that PNNs are also regulated in a circadian and diurnal manner. We sought to determine whether microglia mediate the diurnal regulation of PNNs via CSF1R inhibitor dependent microglial depletion in C57BL/6J mice, and how the absence of microglia might affect cortical diurnal gene expression rhythms. While we observe diurnal differences in microglial morphology, where microglia are most ramified at the onset of the dark phase, we do not find diurnal differences in PNN intensity. However, PNN intensity increases across many brain regions in the absence of microglia, supporting a role for microglia in the regulation of PNNs. Here, we also show that cortical diurnal gene expression rhythms are intact, with no cycling gene changes without microglia. These findings demonstrate a role for microglia in the maintenance of PNNs, but not in the maintenance of diurnal rhythms.
MeSH term(s)	Animals ; Brain Waves/drug effects ; Circadian Rhythm/drug effects ; Circadian Rhythm/genetics ; Circadian Rhythm Signaling Peptides and Proteins/genetics ; Circadian Rhythm Signaling Peptides and Proteins/metabolism ; Gene Expression Regulation ; Male ; Mice, Inbred C57BL ; Microglia/drug effects ; Microglia/metabolism ; Microglia/pathology ; Nerve Net/drug effects ; Nerve Net/metabolism ; Nerve Net/pathology ; Nerve Net/physiopathology ; Organic Chemicals/pharmacology ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/antagonists & inhibitors ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/metabolism ; Somatosensory Cortex/drug effects ; Somatosensory Cortex/metabolism ; Somatosensory Cortex/pathology ; Somatosensory Cortex/physiopathology ; Time Factors ; Mice
Chemical Substances	Circadian Rhythm Signaling Peptides and Proteins ; Csf1r protein, mouse ; Organic Chemicals ; PLX5622 ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor
Language	English
Publishing date	2022-01-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-04079-w
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Article ; Online: To Kill a Microglia: A Case for CSF1R Inhibitors.

Green, Kim N / Crapser, Joshua D / Hohsfield, Lindsay A

Trends in immunology

2020 Volume 41, Issue 9, Page(s) 771–784

Abstract: Microglia, the brain's immune sentinels, have garnered much attention in recent years. Researchers have begun to identify the manifold roles that these cells play in the central nervous system (CNS), and this work has been greatly facilitated by ... ...

Abstract	Microglia, the brain's immune sentinels, have garnered much attention in recent years. Researchers have begun to identify the manifold roles that these cells play in the central nervous system (CNS), and this work has been greatly facilitated by microglial depletion paradigms. The varying degrees of spatiotemporal manipulation afforded by such techniques allow microglial ablation before, during, and/or following insult, injury, or disease. We review the major methods of microglial depletion, including toxin-based, genetic, and pharmacological approaches, which differ in key factors including depletion onset, duration, and off-target effects. We conclude that pharmacological CSF1R inhibitors afford the most extensive versatility in manipulating microglia, making them ideal candidates for future studies investigating microglial function in health and disease.
MeSH term(s)	Central Nervous System/cytology ; Central Nervous System/immunology ; Humans ; Microglia/cytology ; Microglia/immunology ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/antagonists & inhibitors
Chemical Substances	Receptors, Granulocyte-Macrophage Colony-Stimulating Factor
Language	English
Publishing date	2020-08-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2020.07.001
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Zs.A 1601: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Microglia as hackers of the matrix: sculpting synapses and the extracellular space.

Crapser, Joshua D / Arreola, Miguel A / Tsourmas, Kate I / Green, Kim N

Cellular & molecular immunology

2021 Volume 18, Issue 11, Page(s) 2472–2488

Abstract: Microglia shape the synaptic environment in health and disease, but synapses do not exist in a vacuum. Instead, pre- and postsynaptic terminals are surrounded by extracellular matrix (ECM), which together with glia comprise the four elements of the ... ...

Abstract	Microglia shape the synaptic environment in health and disease, but synapses do not exist in a vacuum. Instead, pre- and postsynaptic terminals are surrounded by extracellular matrix (ECM), which together with glia comprise the four elements of the contemporary tetrapartite synapse model. While research in this area is still just beginning, accumulating evidence points toward a novel role for microglia in regulating the ECM during normal brain homeostasis, and such processes may, in turn, become dysfunctional in disease. As it relates to synapses, microglia are reported to modify the perisynaptic matrix, which is the diffuse matrix that surrounds dendritic and axonal terminals, as well as perineuronal nets (PNNs), specialized reticular formations of compact ECM that enwrap neuronal subsets and stabilize proximal synapses. The interconnected relationship between synapses and the ECM in which they are embedded suggests that alterations in one structure necessarily affect the dynamics of the other, and microglia may need to sculpt the matrix to modify the synapses within. Here, we provide an overview of the microglial regulation of synapses, perisynaptic matrix, and PNNs, propose candidate mechanisms by which these structures may be modified, and present the implications of such modifications in normal brain homeostasis and in disease.
MeSH term(s)	Animals ; Brain/immunology ; Extracellular Matrix/metabolism ; Extracellular Space/metabolism ; Humans ; Immunological Synapses/immunology ; Microglia/immunology
Language	English
Publishing date	2021-08-19
Publishing country	China
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2435097-7
ISSN	2042-0226 ; 1672-7681
ISSN (online)	2042-0226
ISSN	1672-7681
DOI	10.1038/s41423-021-00751-3
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Article ; Online: Inflammation in Alzheimer's disease: Lessons learned from microglia-depletion models.

Spangenberg, Elizabeth E / Green, Kim N

Brain, behavior, and immunity

2017 Volume 61, Page(s) 1–11

Abstract: Microglia are the primary immune cell of the brain and function to protect the central nervous system (CNS) from injury and invading pathogens. In the homeostatic brain, microglia serve to support neuronal health through synaptic pruning, promoting ... ...

Abstract	Microglia are the primary immune cell of the brain and function to protect the central nervous system (CNS) from injury and invading pathogens. In the homeostatic brain, microglia serve to support neuronal health through synaptic pruning, promoting normal brain connectivity and development, and through release of neurotrophic factors, providing support for CNS integrity. However, recent evidence indicates that the homeostatic functioning of these cells is lost in neurodegenerative disease, including Alzheimer's disease (AD), ultimately contributing to a chronic neuroinflammatory environment in the brain. Importantly, the development of compounds and genetic models to ablate the microglial compartment has emerged as effective tools to further our understanding of microglial function in AD. Use of these models has identified roles of microglia in several pathological facets of AD, including tau propagation, synaptic stripping, neuronal loss, and cognitive decline. Although culminating evidence utilizing these microglial ablation models reports an absence of CNS-endogenous and peripheral myeloid cell involvement in Aβ phagocytosis, recent data indicates that targeting microglia-evoked neuroinflammation in AD may be essential for potential therapeutics. Therefore, identifying altered signaling pathways in the microglia-devoid brain may assist with the development of effective inflammation-based therapies in AD.
MeSH term(s)	Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Animals ; Brain/metabolism ; Brain/pathology ; Disease Models, Animal ; Inflammation/metabolism ; Inflammation/pathology ; Microglia/metabolism ; Microglia/pathology ; Neurons/metabolism ; Neurons/pathology ; Phagocytosis/physiology ; tau Proteins/metabolism
Chemical Substances	tau Proteins
Language	English
Publishing date	2017-03
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	639219-2
ISSN	1090-2139 ; 0889-1591
ISSN (online)	1090-2139
ISSN	0889-1591
DOI	10.1016/j.bbi.2016.07.003
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Zs.A 2276: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Ablation of microglia following infection of the central nervous system with a neurotropic murine coronavirus infection leads to increased demyelination and impaired remyelination.

Cheng, Yuting / Javonillo, Dominic Ibarra / Pachow, Collin / Scarfone, Vanessa M / Fernandez, Kellie / Walsh, Craig M / Green, Kim N / Lane, Thomas E

Journal of neuroimmunology

2023 Volume 381, Page(s) 578133

Abstract: Intracranial inoculation of susceptible mice with a glial-tropic strain of mouse hepatitis virus (JHMV), a murine coronavirus, results in an acute encephalomyelitis followed by viral persistence in white matter tracts accompanied by chronic ... ...

Abstract	Intracranial inoculation of susceptible mice with a glial-tropic strain of mouse hepatitis virus (JHMV), a murine coronavirus, results in an acute encephalomyelitis followed by viral persistence in white matter tracts accompanied by chronic neuroinflammation and demyelination. Microglia are the resident immune cell of the central nervous system (CNS) and are considered important in regulating events associated with neuroinflammation as well as influencing both white matter damage and remyelination. To better understand mechanisms by which microglia contribute to these immune-mediated events, JHMV-infected mice with established demyelination were treated with the small molecular inhibitor of colony stimulating factor 1 receptor (CSF1R), PLX5622, to deplete microglia. Treatment with PLX5622 did not affect viral replication within the CNS yet the severity of demyelination was increased and remyelination impaired compared to control mice. Gene expression analysis revealed that targeting microglia resulted in altered expression of genes associated with immune cell activation and phagocytosis of myelin debris. These findings indicate that microglia are not critical in viral surveillance in persistently JHMV-infected mice yet restrict white matter damage and remyelination, in part, by influencing phagocytosis of myelin debris.
MeSH term(s)	Mice ; Animals ; Microglia/metabolism ; Murine hepatitis virus/physiology ; Remyelination ; Neuroinflammatory Diseases ; White Matter ; Demyelinating Diseases ; Coronavirus Infections/complications ; Mice, Inbred C57BL
Chemical Substances	PLX5622
Language	English
Publishing date	2023-06-17
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	8335-5
ISSN	1872-8421 ; 0165-5728
ISSN (online)	1872-8421
ISSN	0165-5728
DOI	10.1016/j.jneuroim.2023.578133
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