A new focal model resembling features of cortical pathology of the progressive forms of multiple sclerosis: Influence of innate immunity

Silva, Berenice Anabel; Leal, María Celeste; Farias, Marta Cristina Vieira; Avalos, Juan Carlos Gómez; Besada, Cristina; Pitossi, Fernando Juan; Ferrari, Carina Cintia

doi:10.1016/j.bbi.2018.01.010

Cited by 28 publications

(12 citation statements)

References 109 publications

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“…These pathological features induced cognitive impairment and anxiety-like symptoms in IL-1β injected animals compared to controls. The cortical lesions could be visualized by MRI and the symptoms remained for almost 50 days, demonstrating that it is a chronic model of MS [33] .…”

Section: Focal Demyelinating Lesionmentioning

confidence: 93%

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Neuroinflammation in cortical and meningeal pathology in multiple sclerosis: understanding from animal models

Silva¹,

Miglietta²,

Ferrari³

2020

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Section: Focal Demyelinating Lesionmentioning

confidence: 93%

“…These structures contained CD4+, CD8+, CD20+, CD23+ and CD39+ cells and were associated with cortical demyelination and neurodegeneration along with anxietylike symptoms and short-term memory deterioration. Additionally, these cortico-meningeal structures could be visualized by MRI with gadolinium contrast [33] .…”

Section: Animal Models Of Meningeal Inflammationmentioning

confidence: 99%

Neuroinflammation in cortical and meningeal pathology in multiple sclerosis: understanding from animal models

Silva¹,

Miglietta²,

Ferrari³

2020

Self Cite

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“…EAE mice, before demyelination, exhibit anxiety-and depression-like behaviors and cognitive impairment, which are dependent on the increased IL-1β and TNF-α levels in the hypothalamus [93]. Overexpression of IL-1β leads to MS-like pathologic phenotypes, including neurodegeneration, demyelination, and inflammation, together with cognitive impairments [94].…”

Section: Multiple Sclerosismentioning

confidence: 99%

Inflammasome and Cognitive Symptoms in Human Diseases: Biological Evidence from Experimental Research

Cheon

Kim

et al. 2020

IJMS

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Cognitive symptoms are prevalent in the elderly and are associated with an elevated risk of developing dementia. Disease-driven changes can cause cognitive disabilities in memory, attention, and language. The inflammasome is an innate immune intracellular complex that has a critical role in the host defense system, in that it senses infectious pathogen-associated and endogenous danger-associated molecular patterns. An unbalanced or dysregulated inflammasome is associated with infectious, inflammatory, and neurodegenerative diseases. Due to its importance in such pathological conditions, the inflammasome is an emerging drug target for human diseases. A growing number of studies have revealed links between cognitive symptoms and the inflammasome. Several studies have shown that reducing the inflammasome component mitigates cognitive symptoms in diseased states. Therefore, understanding the inflammasome regulatory mechanisms may be required for the prevention and treatment of cognitive symptoms. The purpose of this review is to discuss the current understanding of the inflammasome and its relationships with cognitive symptoms in various human diseases.

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“…19 Long-term application of cuprizone induces chronic demyelination, 20 and it is the best model for assessment of both remyelination and oligodendrocyte cell death. 21 Available drugs are able to suppress inflammation and to protect neurons from the subsequent events, namely demyelination and axonal damage, but they could not influence remyelination and repair systems. In this study, we investigate the effects of the CSF1R inhibitor PLX3397 (used as a microglial depletion drug) in a cuprizone-induced corpus callosum demyelination in mice.…”

Section: Introductionmentioning

confidence: 99%

“…Remyelination is considered as one of the most efficient repair processes within the CNS for sustaining structural integrity of axons and restoring axonal conduction properties following the exposure to a demyelinated insult . Long‐term application of cuprizone induces chronic demyelination, and it is the best model for assessment of both remyelination and oligodendrocyte cell death . Available drugs are able to suppress inflammation and to protect neurons from the subsequent events, namely demyelination and axonal damage, but they could not influence remyelination and repair systems.…”

Section: Introductionmentioning

confidence: 99%

Effect of the CSF1R inhibitor PLX3397 on remyelination of corpus callosum in a cuprizone‐induced demyelination mouse model

Tahmasebi

Pasbakhsh

Mortezaee

et al. 2019

J of Cellular Biochemistry

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Multiple sclerosis (MS) is a chronic inflammatory disease affecting the central nervous system (CNS). Despite introducing multiple immunomodulatory approaches for MS, there are still major concerns about possible ways for improving remyelination in this disease. Microglia exert essential roles in regulation of myelination processes, and interaction between colony-stimulating factor 1 (CSF1) with its receptor CSF1R is considered as a key regulator of microglial differentiation and survival. The aim of this study was to investigate possible roles for a CSF1R inhibitor PLX3397 in recovery of central myelination processes. Chronic demyelination was induced in mice by addition of 0.2% cuprizone to the chow for 12 weeks. Next, animals were undergoing a diet containing 290 mg/kg PLX3397 to induce microglial ablation. The PLX3397 treatment caused a significant decrease in the rate of expression for the CSF1/CSF1R axis, and a reduction in the protein expressions for the microglial marker Iba-1 and for the oligodendrocyte marker Olig-2. Findings from Luxol fast blue (LFB) staining and transmission electron microscopy (TEM) showed an increase in the rate of myelination for the mice receiving PLX3397. The rate of destruction in the nerve fibers and the extent of the gaps formed between layers of myelin sheaths was also reduced after the treatment with PLX3397. In addition, animals experienced an improvement in recovery of motor deficit after receiving PLX3397 (for all P < 0.05). It could be concluded that PLX3397 could retain myelination in the MS model possibly through regulation of the myelin environment. K E Y W O R D Scolony-stimulating factor 1 (CSF1), CSF1R, cuprizone, demyelination, microglia, multiple sclerosis (MS), PLX3397 Effect of the CSF1R inhibitor PLX3397 on remyelination of corpus callosum in a cuprizoneinduced demyelination mouse model.

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A new focal model resembling features of cortical pathology of the progressive forms of multiple sclerosis: Influence of innate immunity

Cited by 28 publications

References 109 publications

Neuroinflammation in cortical and meningeal pathology in multiple sclerosis: understanding from animal models

Neuroinflammation in cortical and meningeal pathology in multiple sclerosis: understanding from animal models

Inflammasome and Cognitive Symptoms in Human Diseases: Biological Evidence from Experimental Research

Effect of the CSF1R inhibitor PLX3397 on remyelination of corpus callosum in a cuprizone‐induced demyelination mouse model

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