The Relationship Between Serum S100B Levels And Microglial Activation In Rat Hipocampus After Lithium-pilocarpine Induced Status Epilepticus And The Effect Of Liraglutide, A GLP-1 Analogue On These Changes

2017 ◽  
Author(s):  
Sevda Muftuoglu
Keyword(s):  
Status Epilepticus ◽  
Microglial Activation ◽  
Serum S100b ◽  
The Relationship

scholarly journals The relationship between CD204 M2-polarized tumour-associated macrophages (TAMs), tumour-infiltrating lymphocytes (TILs), and microglial activation in glioblastoma microenvironment: a novel immune checkpoint receptor target

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Maher Kurdi ◽  
Badrah Alghamdi ◽  
Nadeem Shafique Butt ◽  
Saleh Baeesa
Keyword(s):  
Microglial Activation ◽  
Inverse Correlation ◽  
Idh1 Mutation ◽  
High Expression ◽  
Kaplan Meier ◽  
Significant Difference ◽  
Tumour Infiltrating Lymphocytes ◽  
Infiltrating Lymphocytes ◽  
The Relationship ◽  
Low Expression

Abstract Background Tumour associated macrophages (TAMs) and tumour infiltrating lymphocytes (TILs) are considered dominant cells in glioblastoma microenvironment. Aim The purpose of this study was to assess the expression of CD204+ M2-polarized TAMs in glioblastomas and their relationship with CD4+TILs, Iba+microglia, and IDH1 mutation. We also exploreed the prognostic value of these markers on the recurrence-free interval (RFI). Methods The expressions of CD204+TAMs, CD4+TILs, and Iba1+microglia were quantitively assessed in 45 glioblastomas using immunohistochemistry. Kaplan–Meier analysis and Cox hazards were used to examine the relationship between these factors. Results CD204+TAMs were highly expressed in 32 tumours (71%) and the remaining 13 tumours (29%) had reduced expression. CD4+TILs were highly expressed in 10 cases (22%) and 35 cases (77.8%) had low expression. There was an inverse correlation between CD204+TAMs and CD4+TILs, in which 85% of tumours had a high expression of CD204+TAMs and a low expression of CD4+TILs. Nevertheless, there was no significant difference in IDH1 mutation status between the two groups (p = 0.779). There was a significant difference in Iba1+microglial activation between IDH1mutant and IDH1wildtype groups (p = 0.031). For cases with a high expression of CD204+TAMs and a low expression of CD4+TILs, there was a significant difference in RFI after treatment with chemoradiotherapy or radiotherapy (p = 0.030). Conclusion Glioblastoma with a dense CD204+TAMs and few CD4+TILs is associated with IDH1wildtype. These findings suggest that TAMs masks tumour cell and suppress T-cell tumoricidal functions via immunomodulatory mechanisms. Blockade of the CD204-TAM receptor may prevent this mechanism and allow the evolution of TILs.

scholarly journals Microglial Phenotypes and Their Relationship to the Cannabinoid System: Therapeutic Implications for Parkinson’s Disease

Molecules ◽  
2020 ◽  
Vol 25 (3) ◽  
pp. 453 ◽  
Author(s):  
Rachel Kelly ◽  
Valerie Joers ◽  
Malú G. Tansey ◽  
Declan P. McKernan ◽  
Eilís Dowd
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Microglial Activation ◽  
Cannabinoid Receptors ◽  
Neurodegenerative Disorder ◽  
Therapeutic Benefit ◽  
Cannabinoid System ◽  
Therapeutic Implications ◽  
Microglial Phenotype ◽  
The Relationship

Parkinson’s disease is a neurodegenerative disorder, the motor symptoms of which are associated classically with Lewy body formation and nigrostriatal degeneration. Neuroinflammation has been implicated in the progression of this disease, by which microglia become chronically activated in response to α-synuclein pathology and dying neurons, thereby acquiring dishomeostatic phenotypes that are cytotoxic and can cause further neuronal death. Microglia have a functional endocannabinoid signaling system, expressing the cannabinoid receptors in addition to being capable of synthesizing and degrading endocannabinoids. Alterations in the cannabinoid system—particularly an upregulation in the immunomodulatory CB2 receptor—have been demonstrated to be related to the microglial activation state and hence the microglial phenotype. This paper will review studies that examine the relationship between the cannabinoid system and microglial activation, and how this association could be manipulated for therapeutic benefit in Parkinson’s disease.

scholarly journals The Relationship Between Serial [18 F]PBR06 PET Imaging of Microglial Activation and Motor Function Following Stroke in Mice

2014 ◽  
Vol 16 (6) ◽  
pp. 821-829 ◽  
Author(s):  
Frederick M. Lartey ◽  
G-One Ahn ◽  
Rehan Ali ◽  
Sahar Rosenblum ◽  
Zheng Miao ◽  
...  
Keyword(s):  
Motor Function ◽  
Pet Imaging ◽  
Microglial Activation ◽  
The Relationship

scholarly journals Risk factors for malnutrition in refractory convulsive status epilepticus

2020 ◽  
Author(s):  
Yu Zhang ◽  
Deng Chen ◽  
Li-na Zhu ◽  
ling liu
Keyword(s):  
Risk Factors ◽  
Logistic Regression ◽  
Status Epilepticus ◽  
Logistic Regression Model ◽  
Adverse Outcomes ◽  
Convulsive Status Epilepticus ◽  
Common Complication ◽  
West China Hospital ◽  
West China ◽  
The Relationship

Abstract Purpose: To study the risk factors and prognosis of malnutrition in patients with refractory convulsive status epilepticus. Methods: A total of 73 patients with refractory convulsive epileptic status in West China Hospital from January 2017 to May 2019 were collected. All patients met the 2016 International Anti-epileptic Alliance diagnostic criteria for refractory convulsive status epilepticus. A logistic regression model was used to evaluate the risk factors of malnutrition in refractory convulsive status epilepticus. Results: Of the 73 patients with refractory convulsive status epilepticus, 33 (45.21%) suffered from malnutrition during hospitalization, and hospitalization days (OR =1.251; 95% CI: 1.067-1.384; P =0.007), nasal feeding (OR =22.623; 95% CI: 1.091-286.899; P =0.013), and malnutrition on admission (OR =30.760; 95% CI: 1.064-89.797; P =0.046) were risk factors for malnutrition in patients with refractory convulsive status epilepticus. Conclusion: Malnutrition is a common complication during hospitalization in patients with refractory convulsive status epilepticus. Hospitalization days, nasal feeding, and malnutrition at admission are risk factors for malnutrition in patients with refractory convulsive status epilepticus. Further longitudinal studies are needed to identify the relationship between refractory convulsive status epilepticus and adverse outcomes.

scholarly journals Dysregulated phosphoinositide 3-kinase signaling in microglia: shaping chronic neuroinflammation

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Erskine Chu ◽  
Richelle Mychasiuk ◽  
Margaret L. Hibbs ◽  
Bridgette D. Semple
Keyword(s):  
Neurodegenerative Disease ◽  
Microglial Activation ◽  
Protein Kinase B ◽  
Disease Onset ◽  
Akt Signaling ◽  
Phosphatidylinositol 3 Kinase ◽  
Chronic Neuroinflammation ◽  
Promising Therapeutic Approach ◽  
Phosphoinositide 3 Kinase ◽  
The Relationship

AbstractMicroglia are integral mediators of innate immunity within the mammalian central nervous system. Typical microglial responses are transient, intending to restore homeostasis by orchestrating the removal of pathogens and debris and the regeneration of damaged neurons. However, prolonged and persistent microglial activation can drive chronic neuroinflammation and is associated with neurodegenerative disease. Recent evidence has revealed that abnormalities in microglial signaling pathways involving phosphatidylinositol 3-kinase (PI3K) and protein kinase B (AKT) may contribute to altered microglial activity and exacerbated neuroimmune responses. In this scoping review, the known and suspected roles of PI3K-AKT signaling in microglia, both during health and pathological states, will be examined, and the key microglial receptors that induce PI3K-AKT signaling in microglia will be described. Since aberrant signaling is correlated with neurodegenerative disease onset, the relationship between maladapted PI3K-AKT signaling and the development of neurodegenerative disease will also be explored. Finally, studies in which microglial PI3K-AKT signaling has been modulated will be highlighted, as this may prove to be a promising therapeutic approach for the future treatment of a range of neuroinflammatory conditions.

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