Microglia: Lifelong modulator of neural circuits

Ikegami, Ako; Haruwaka, Koichiro

doi:10.1111/neup.12560

Cited by 46 publications

(30 citation statements)

References 68 publications

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“…Microglial cells play a key role in the maintenance of brain homeostasis from early development to adulthood, including neurodevelopment, synaptic pruning, neuronal circuit maturation [ 20 , 21 ], and the impairment of microglial functions which can lead to severe pathological outcomes.…”

Section: Microglia Function In Health and Prion Diseasesmentioning

confidence: 99%

Microglia in Prion Diseases: Angels or Demons?

Peggion

Stella

Lorenzon

et al. 2020

IJMS

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Prion diseases are rare transmissible neurodegenerative disorders caused by the accumulation of a misfolded isoform (PrPSc) of the cellular prion protein (PrPC) in the central nervous system (CNS). Neuropathological hallmarks of prion diseases are neuronal loss, astrogliosis, and enhanced microglial proliferation and activation. As immune cells of the CNS, microglia participate both in the maintenance of the normal brain physiology and in driving the neuroinflammatory response to acute or chronic (e.g., neurodegenerative disorders) insults. Microglia involvement in prion diseases, however, is far from being clearly understood. During this review, we summarize and discuss controversial findings, both in patient and animal models, suggesting a neuroprotective role of microglia in prion disease pathogenesis and progression, or—conversely—a microglia-mediated exacerbation of neurotoxicity in later stages of disease. We also will consider the active participation of PrPC in microglial functions, by discussing previous reports, but also by presenting unpublished results that support a role for PrPC in cytokine secretion by activated primary microglia.

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Section: Microglia Function In Health and Prion Diseasesmentioning

confidence: 99%

Microglia in Prion Diseases: Angels or Demons?

Peggion

Stella

Lorenzon

et al. 2020

IJMS

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“…As the sole immune cells in the brain, microglia play essential roles in maintaining brain functions by plays sentinel, housekeeping function and defense roles (Wolf et al, 2017;Hickman et al, 2018). Microglia strongly influence the pathologic outcomes in non-infectious pathological states (Ramirez et al, 2017;Ikegami et al, 2019) and acts as pivotal mediators of neuroinflammation via the release of cytokines, chemokines, and growth factors in various infectious diseases to regulate innate immunity and participate in adaptive immune responses in CNS tissue (Colonna and Butovsky, 2017). Our previous work indicated that microglial activation, which is considered a main target for therapeutic interventions for a variety of CNS diseases (Heppner et al, 2005;Garden and Möller, 2006), appears to be one of the checkpoints in CNS inflammation caused by A. cantonensis infection (Zhao et al, 2013;Wei et al, 2015), and the administration of minocycline, an inhibitor of microglial activation, is effective in treating mice infected with A. cantonensis (unpublished data).…”

Section: Discussionmentioning

confidence: 99%

Necroptosis and Caspase-2-Mediated Apoptosis of Astrocytes and Neurons, but Not Microglia, of Rat Hippocampus and Parenchyma Caused by Angiostrongylus cantonensis Infection

et al. 2020

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Zhou et al. Lv's Manuscript in Frontiers in Microbiology obvious, suggesting that apoptosis and necroptosis but not autophagy or pyroptosis occurred in the brains of infected animals at 21 and 28 dpi. The results of RT-qPCR, western blot analysis, IF, flow cytometry and TEM further illustrated that necroptosis and caspase-2-mediated apoptosis occurred in astrocytes and neurons but not in microglia in the parenchyma and hippocampus of infected animals. This study provides the first evidence that neuronal and astrocytic necroptosis and caspase-2-mediated apoptosis are induced by A. cantonensis infection in the parenchymal and hippocampal regions of rats at 21 and 28 dpi but these processes are negligible at 35 dpi. These findings enhance our understanding of the pathogenesis of A. cantonensis infection and provide new insights into therapeutic approaches targeting the occurrence of cell death in astrocytes and neurons in infected patients.

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“…However, synaptic plasticity does not only involve only neurons but also interactions with glial cells such as astrocytes and microglia [162]. Microglia are key regulator of neurodevelopment, neuroinflammation, and BBB integrity [167]. An important mechanism involved in cognition is microglia-dependent synaptic removal, which allows synapse remodeling called synapse pruning [167].…”

Section: Arbovirus and Modulation Of Synaptic Functionmentioning

confidence: 99%

“…Microglia are key regulator of neurodevelopment, neuroinflammation, and BBB integrity [167]. An important mechanism involved in cognition is microglia-dependent synaptic removal, which allows synapse remodeling called synapse pruning [167]. This mechanism, when exacerbated, can cause cognitive dysfunction [168,169].…”

Section: Arbovirus and Modulation Of Synaptic Functionmentioning

confidence: 99%

Neurocognitive impacts of arbovirus infections

Clé

Eldin

Briant

et al. 2020

J Neuroinflammation

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Arthropod-borne viruses or arbovirus, are most commonly associated with acute infections, resulting on various symptoms ranging from mild fever to more severe disorders such as hemorrhagic fever. Moreover, some arboviral infections can be associated with important neuroinflammation that can trigger neurological disorders including encephalitis, paralysis, ophthalmological impairments, or developmental defects, which in some cases, can lead to long-term defects of the central nervous system (CNS). This is well illustrated in Zika virus-associated congenital brain malformations but also in West Nile virus-induced synaptic dysfunctions that can last well beyond infection and lead to cognitive deficits. Here, we summarize clinical and mechanistic data reporting on cognitive disturbances triggered by arboviral infections, which may highlight growing public health issues spanning the five continents.

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Microglia: Lifelong modulator of neural circuits

Cited by 46 publications

References 68 publications

Microglia in Prion Diseases: Angels or Demons?

Microglia in Prion Diseases: Angels or Demons?

Necroptosis and Caspase-2-Mediated Apoptosis of Astrocytes and Neurons, but Not Microglia, of Rat Hippocampus and Parenchyma Caused by Angiostrongylus cantonensis Infection

Neurocognitive impacts of arbovirus infections

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