Neuroinflammation

Mukhara, Deepika; Oh, Unsong; Neigh, Gretchen N.

doi:10.1016/b978-0-444-64123-6.00017-5

Cited by 31 publications

(19 citation statements)

References 269 publications

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“…Diseases with an autoimmune component such as optic neuromyelitis and multiple sclerosis [2], aging and obesity [3] can also be considered triggers of inflammation. Accumulating evidence suggests that neuroinflammation plays an important role in the etiology of mental disorders, a variety of neurological and somatic diseases, including epilepsy, Alzheimer's disease, Parkinson's disease, autism spectrum disorders, bipolar disorder, affective disorders, depression [4][5][6][7][8] and systemic lupus erythematosus [9,10]. Recent data suggests that neuroinflammation is one of the key processes in glaucoma and retinopathy [11][12][13][14], it is also important in the pathogenesis of heart failure [15].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of Drug Resistance in the Pathogenesis of Epilepsy: Role of Neuroinflammation. A Literature Review

2021

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Epilepsy is a chronic neurological disorder characterized by recurring spontaneous seizures. Drug resistance appears in 30% of patients and it can lead to premature death, brain damage or a reduced quality of life. The purpose of the study was to analyze the drug resistance mechanisms, especially neuroinflammation, in the epileptogenesis. The information bases of biomedical literature Scopus, PubMed, Google Scholar and SciVerse were used. To obtain full-text documents, electronic resources of PubMed Central and Research Gate were used. The article examines the recent research of the mechanisms of drug resistance in epilepsy and discusses the hypotheses of drug resistance development (genetic, epigenetic, target hypothesis, etc.). Drug-resistant epilepsy is associated with neuroinflammatory, autoimmune and neurodegenerative processes. Neuroinflammation causes immune, pathophysiological, biochemical and psychological consequences. Focal or systemic unregulated inflammatory processes lead to the formation of aberrant neural connections and hyperexcitable neural networks. Inflammatory mediators affect the endothelium of cerebral vessels, destroy contacts between endothelial cells and induce abnormal angiogenesis (the formation of “leaky” vessels), thereby affecting the blood–brain barrier permeability. Thus, the analysis of pro-inflammatory and other components of epileptogenesis can contribute to the further development of the therapeutic treatment of drug-resistant epilepsy.

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Section: Introductionmentioning

confidence: 99%

Mechanisms of Drug Resistance in the Pathogenesis of Epilepsy: Role of Neuroinflammation. A Literature Review

2021

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“…Moreover, being attracted by the factors released from damaged cells, microglia exhibit enhanced motility toward the sites of injury, which is one of the common features of chronic inflammation during the early phases of neurodegeneration [6]. Accumulating evidence indicates that neuroinflammation is implicated in the principal pathogenesis of a variety of neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD) [7].…”

Section: Introductionmentioning

confidence: 99%

Suppression of LPS-Induced Inflammation and Cell Migration by Azelastine through Inhibition of JNK/NF-κB Pathway in BV2 Microglial Cells

Nguyen

Bui

Duong

et al. 2021

IJMS

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The c-Jun N-terminal kinases (JNKs) are implicated in many neuropathological conditions, including neurodegenerative diseases. To explore potential JNK3 inhibitors from the U.S. Food and Drug Administration-approved drug library, we performed structure-based virtual screening and identified azelastine (Aze) as one of the candidates. NMR spectroscopy indicated its direct binding to the ATP-binding site of JNK3, validating our observations. Although the antihistamine effect of Aze is well documented, the involvement of the JNK pathway in its action remains to be elucidated. This study investigated the effects of Aze on lipopolysaccharide (LPS)-induced JNK phosphorylation, pro-inflammatory mediators, and cell migration in BV2 microglial cells. Aze was found to inhibit the LPS-induced phosphorylation of JNK and c-Jun. It also inhibited the LPS-induced production of pro-inflammatory mediators, including interleukin-6, tumor necrosis factor-α, and nitric oxide. Wound healing and transwell migration assays indicated that Aze attenuated LPS-induced BV2 cell migration. Furthermore, Aze inhibited LPS-induced IκB phosphorylation, thereby suppressing nuclear translocation of NF-κB. Collectively, our data demonstrate that Aze exerts anti-inflammatory and anti-migratory effects through inhibition of the JNK/NF-κB pathway in BV2 cells. Based on our findings, Aze may be a potential candidate for drug repurposing to mitigate neuroinflammation in various neurodegenerative disorders, including Alzheimer’s and Parkinson’s diseases.

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“…In response to the question of stressed-mice showing significant increase in toll-like receptor 4 (TLR4) and whether humans would have the same effect, the expert stated that "TLR4 is one of the major receptors that is responsible for the neuroimmune system… activation of the TLR4 will activate the neuroimmunity cells in the nervous system that will bring about the emergence of neuroinflammation". Neuroinflammation is the activation of the brain's innate immune system in response to an inflammatory challenge (Milatovic et al, 2017) and if left untreated could lead to several psychosomatic and neurological illness such as depression (Mukhara et al, 2020). To another supplementary question on whether lipopolysaccharide-rhodobacter sphaeroides (LPS-RS) can be used on humans since treated stressed-mice showed a significant decrease in ethanol drinking, the expert postulated that although "LPS-RS is a synthesized laboratory drug that can only be used safely on animal models, studies have shown that humans are able to naturally produce certain chemical components in the body that possess similar suppressing effect of LPS-RS on TLR4 that are observable in behavioral changes which is the adaptation of the stress level".…”

Section: Interview Resultsmentioning

confidence: 99%

Online Learning Motivation During Covid-19 Pandemic

Yong

Thi

2022

Malaysian Journal of Learning and Instruction

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Purpose - Due to the COVID-19 pandemic, the Malaysian government declared a Movement Control Order (MCO) to prevent the spread of the virus. Educational institutions were forced to switch their pedagogy to online learning to complete the semester curriculum, catching academicians and students off-guard that resulted in makeshift online lesson delivery. Previous online learning motivation studies have neglected the impact of an unplanned or sudden transition to online learning during a pandemic on student motivation to learn. This study aims to examine location learning environment, learner-instructor interactions, and self-efficacy of students more succinctly on their learning motivation during an unplanned transition to online learning. Method - This study used a sequential explanatory mixed method strategy with a sample size of 535 randomly collected from a public and two private higher education institutions in Malaysia. IBM SPSS statistical software v22 was used for descriptive statistics. Regression testing was carried out using AMOS statistical software v21 structural equation modeling. Findings - Revealed the importance of location learning environment in fostering student motivation and the positive influence of learner-instructor interactions on students achieving the desired learning outcomes during an unplanned transition to online learning. However, there is no evidence to suggest a causal effect between student self-efficacy and online learning motivation during such conditions. The theoretical implication indicates that having conducive hygiene factors are essential to driving student motivation under such situations. Significance - The COVID-19 pandemic provides opportunities for researchers to examine the role of various motivational theories to explain student motivation in learning under challenging conditions. Educators and students would benefit on ways to increase student online learning motivation in lockdown conditions. Setting up a more efficient online delivery approach could lead to higher student satisfaction and potential enrolment.

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Neuroinflammation

Cited by 31 publications

References 269 publications

Mechanisms of Drug Resistance in the Pathogenesis of Epilepsy: Role of Neuroinflammation. A Literature Review

Mechanisms of Drug Resistance in the Pathogenesis of Epilepsy: Role of Neuroinflammation. A Literature Review

Suppression of LPS-Induced Inflammation and Cell Migration by Azelastine through Inhibition of JNK/NF-κB Pathway in BV2 Microglial Cells

Online Learning Motivation During Covid-19 Pandemic

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