Adenosine Receptors in Modulation of Central Nervous System Disorders

2019 ◽  
Vol 25 (26) ◽  
pp. 2808-2827 ◽  
Author(s):  
Hira Choudhury ◽  
Dinesh K. Chellappan ◽  
Pallav Sengupta ◽  
Manisha Pandey ◽  
Bapi Gorain
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adenosine Receptors ◽  
Drug Targets ◽  
Active Components ◽  
Cns Disorders ◽  
The Central Nervous System ◽  
Minimal Concentration ◽  
The Impact ◽  
G Protein Coupled

The ubiquitous signaling nucleoside molecule, adenosine is found in different cells of the human body to provide its numerous pharmacological role. The associated actions of endogenous adenosine are largely dependent on conformational change of the widely expressed heterodimeric G-protein-coupled A1, A2A, A2B, and A3 adenosine receptors (ARs). These receptors are well conserved on the surface of specific cells, where potent neuromodulatory properties of this bioactive molecule reflected by its easy passage through the rigid blood-brainbarrier, to simultaneously act on the central nervous system (CNS). The minimal concentration of adenosine in body fluids (30–300 nM) is adequate to exert its neuromodulatory action in the CNS, whereas the modulatory effect of adenosine on ARs is the consequence of several neurodegenerative diseases. Modulatory action concerning the activation of such receptors in the CNS could be facilitated towards neuroprotective action against such CNS disorders. Our aim herein is to discuss briefly pathophysiological roles of adenosine on ARs in the modulation of different CNS disorders, which could be focused towards the identification of potential drug targets in recovering accompanying CNS disorders. Researches with active components with AR modulatory action have been extended and already reached to the bedside of the patients through clinical research in the improvement of CNS disorders. Therefore, this review consist of recent findings in literatures concerning the impact of ARs on diverse CNS disease pathways with the possible relevance to neurodegeneration.

scholarly journals The Roles of Lpar1 in Central Nervous System Disorders and Diseases

2021 ◽  
Vol 15 ◽  
Author(s):  
Dongqiong Xiao ◽  
Xiaojuan Su ◽  
Hu Gao ◽  
Xihong Li ◽  
Yi Qu
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cell Types ◽  
Potential Therapeutic Target ◽  
Cns Disorders ◽  
The Central Nervous System ◽  
Almost All ◽  
G Protein Coupled ◽  
Differentiation Gene ◽  
The Brain

Lysophosphatidic acid receptor 1 (Lpar1), which is found in almost all human tissues but is most abundant in the brain, can couple to G protein-coupled receptors (GPCRs) and participate in regulating cell proliferation, migration, survival, and apoptosis. Endothelial differentiation gene-2 receptor (Edg2), the protein encoded by the Lpar1 gene, is present on various cell types in the central nervous system (CNS), such as neural stem cells (NSCs), oligodendrocytes, neurons, astrocytes, and microglia. Lpar1 deletion causes neurodevelopmental disorders and CNS diseases, such as brain cancer, neuropsychiatric disorders, demyelination diseases, and neuropathic pain. Here, we summarize the possible roles and mechanisms of Lpar1/Edg2 in CNS disorders and diseases and propose that Lpar1/Edg2 might be a potential therapeutic target for CNS disorders and diseases.

scholarly journals The variable monoaminergic outcomes of cleaner fish brains when facing different social and mutualistic contexts

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e4830 ◽  
Author(s):  
Murilo S. de Abreu ◽  
João P.M. Messias ◽  
Per-Ove Thörnqvist ◽  
Svante Winberg ◽  
Marta C. Soares
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Social Behaviour ◽  
Visual Assessment ◽  
Physical Contact ◽  
Specific Response ◽  
Dopaminergic Activity ◽  
Cleaner Fish ◽  
The Central Nervous System ◽  
The Impact

The monoamines serotonin and dopamine are important neuromodulators present in the central nervous system, known to be active regulators of social behaviour in fish as in other vertebrates. Our aim was to investigate the region-specific brain monoaminergic differences arising when individual cleaners face a client (mutualistic context) compared to when they are introduced to another conspecific (conspecific context), and to understand the relevance of visual assessment compared to the impact of physical contact with any partner. We demonstrated that serotoninergic activity at the diencephalon responds mostly to the absence of physical contact with clients whereas cerebellar dopaminergic activity responds to actual cleaning engagement. We provide first insights on the brain’s monoaminergic (region-specific) response variations, involved in the expression of cleaner fishes’ mutualistic and conspecific behaviour. These results contribute to a better understanding of the monoaminergic activity in accordance to different socio-behavioural contexts.

scholarly journals Progress in Research on SARS-CoV-2 Infection Causing Neurological Diseases and Its Infection Mechanism

2021 ◽  
Vol 11 ◽  
Author(s):  
Lintao Wang ◽  
Zhiguang Ren ◽  
Li Ma ◽  
Yanjie Han ◽  
Wenqiang Wei ◽  
...  
Keyword(s):  
Public Health ◽  
Central Nervous System ◽  
Nervous System ◽  
Neurological Diseases ◽  
Public Health Problem ◽  
Neurological Complications ◽  
Major Public Health Problem ◽  
The Central Nervous System ◽  
The Impact ◽  
Great Harm

COVID-19 has spread rapidly worldwide since its outbreak and has now become a major public health problem. More and more evidence indicates that SARS-CoV-2 may not only affect the respiratory system but also cause great harm to the central nervous system. Therefore, it is extremely important to explore in-depth the impact of SARS-CoV-2 infection on the nervous system. In this paper, the possible mechanisms of SARS-CoV-2 invading the central nervous system during COVID-19, and the neurological complications caused by SARS-CoV-2 infection were reviewed.

Relation of insulin resistance to neurocognitive function and electroencephalography in obese children

2017 ◽  
Vol 30 (10) ◽  
Author(s):  
Onur Akın ◽  
İbrahim Eker ◽  
Mutluay Arslan ◽  
Süleyman Tolga Yavuz ◽  
Sevil Akman ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Central Nervous System ◽  
Nervous System ◽  
Healthy Children ◽  
Model Assessment ◽  
Obese Children ◽  
Neurocognitive Functions ◽  
The Central Nervous System ◽  
Biochemical Indices ◽  
The Impact

AbstractBackground:Childhood obesity may lead to neuronal impairment in both the peripheral and the central nervous system. This study aimed to investigate the impact of obesity and insulin resistance (IR) on the central nervous system and neurocognitive functions in children.Methods:Seventy-three obese children (38 male and 35 female) and 42 healthy children (21 male and 21 female) were recruited. Standard biochemical indices and IR were evaluated. The Wechsler Intelligence Scale for Children-Revised (WISC-R) and electroencephalography (EEG) were administered to all participants. The obese participants were divided into two groups based on the presence or absence of IR, and the data were compared between the subgroups.Results:Only verbal scores on the WISC-R in the IR+ group were significantly lower than those of the control and IR– groups. There were no differences between the groups with respect to other parameters of the WISC-R or the EEG. Verbal scores of the WISC-R were negatively correlated with obesity duration and homeostatic model assessment-insulin resistance (HOMA-IR) values. EEGs showed significantly more frequent ‘slowing during hyperventilation’ (SDHs) in obese children than non-obese children.Conclusions:Neurocognitive functions, particularly verbal abilities, were impaired in obese children with IR. An early examination of cognitive functions may help identify and correct such abnormalities in obese children.

HLA-DRB1*1501 intensifies the impact of IL-6 promoter polymorphism on the susceptibility to multiple sclerosis in an Iranian population

2010 ◽  
Vol 16 (10) ◽  
pp. 1173-1177 ◽  
Author(s):  
M. Shahbazi ◽  
H. Ebadi ◽  
D. Fathi ◽  
D. Roshandel ◽  
M. Mohamadhosseni ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Promoter Polymorphism ◽  
Exact Test ◽  
Inflammatory Processes ◽  
The Central Nervous System ◽  
Pcr Method ◽  
Multiple Sclerosis Patients ◽  
The Impact

Background: The multifunctional cytokine interleukin-6 (IL-6) is involved in inflammatory processes in the central nervous system. It is well documented that amount of IL-6 is increased in serum, cerebrospinal fluid and central nervous system lesions of patients with multiple sclerosis. A single nucleotide polymorphism at position -174 in the IL-6 gene promotor appears to influence IL-6 expression. Recently, several researchers have focused on HLA-DRB alleles, specifically HLA-DRB1*1501, as a potential risk allele in the pathogenesis of multiple sclerosis. Objective: To investigate the possible influence of IL-6/-174 polymorphisms on susceptibility to multiple sclerosis and its integration with HLA-DRB1*1501. Genomic DNA was extracted from whole blood of 345 patients with multiple sclerosis and 426 control subjects. Method: The SSP-PCR method was used to determine genotypes and Fisher’s exact test was applied to determine differences between groups. HLA-DRB1*1501 was observed more frequently among multiple sclerosis patients compared with healthy subjects (45% and 34%, respectively; OR = 1.6, 95% CI = 1.2—2.2, p = 0.0018). At the IL-6/-174 position, the G allele had higher frequency among multiple sclerosis patients compared with controls (77% and 70%, respectively; OR = 1.4, 95% CI = 1.1—1.8, p = 0.0038). This difference was more significant among HLA-DRB1*1501-positive patients and controls (81% and 67%, respectively; OR = 1.9, 95% CI = 1.5—2.5, p < 0.0001). Results: Our results have shown that the G allele at the IL-6/-174 promoter polymorphism may be associated with development of multiple sclerosis in this population, and may be strengthened by HLA-DRB1*1501. Conclusions: We suggest more studies to confirm these results in other populations.

scholarly journals The impact of high and low dose ionising radiation on the central nervous system

Redox Biology ◽  
2016 ◽  
Vol 9 ◽  
pp. 144-156 ◽  
Author(s):  
Calina Betlazar ◽  
Ryan J. Middleton ◽  
Richard B. Banati ◽  
Guo-Jun Liu
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Low Dose ◽  
Ionising Radiation ◽  
The Central Nervous System ◽  
The Impact

scholarly journals Neuroinflammation as Fuel for Axonal Regeneration in the Injured Vertebrate Central Nervous System

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Ilse Bollaerts ◽  
Jessie Van houcke ◽  
Lien Andries ◽  
Lies De Groef ◽  
Lieve Moons
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Axonal Regeneration ◽  
Current Knowledge ◽  
Cord Injury ◽  
The Central Nervous System ◽  
Novel Therapeutic Strategies ◽  
The Impact ◽  
Vertebrate Central Nervous System

Damage to the central nervous system (CNS) is one of the leading causes of morbidity and mortality in elderly, as repair after lesions or neurodegenerative disease usually fails because of the limited capacity of CNS regeneration. The causes underlying this limited regenerative potential are multifactorial, but one critical aspect is neuroinflammation. Although classically considered as harmful, it is now becoming increasingly clear that inflammation can also promote regeneration, if the appropriate context is provided. Here, we review the current knowledge on how acute inflammation is intertwined with axonal regeneration, an important component of CNS repair. After optic nerve or spinal cord injury, inflammatory stimulation and/or modification greatly improve the regenerative outcome in rodents. Moreover, the hypothesis of a beneficial role of inflammation is further supported by evidence from adult zebrafish, which possess the remarkable capability to repair CNS lesions and even restore functionality. Lastly, we shed light on the impact of aging processes on the regenerative capacity in the CNS of mammals and zebrafish. As aging not only affects the CNS, but also the immune system, the regeneration potential is expected to further decline in aged individuals, an element that should definitely be considered in the search for novel therapeutic strategies.

scholarly journals Drp1 is widely, yet heterogeneously, distributed in the mouse central nervous system

2020 ◽  
Author(s):  
Ting-Ting Luo ◽  
Chun-Qiu Dai ◽  
Jia-Qi Wang ◽  
Zheng-Mei Wang ◽  
Yi Yang ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Malignant Glioma ◽  
Expression Patterns ◽  
Heterogeneous Distribution ◽  
Human Malignant Glioma ◽  
The Central Nervous System ◽  
The Impact ◽  
The Relationship ◽  
Mouse Central Nervous System

Abstract Objectives: Drp1 is widely expressed in the mouse central nervous system and plays a role in inducing the mitochondrial fission process. Many diseases are associated with Drp1 and mitochondria. However, since the exact distribution of Drp1 has not been specifically observed, it is difficult to determine the impact of anti-Drp1 molecules on the human body. Clarifying the specific Drp1 distribution could be a good approach to targeted treatment or prognosis. Methods: We visualized the distribution of Drp1 in different brain regions and explicated the relationship between Drp1 and mitochondria. GAD67-GFP knock-in mice were utilized to detect the expression patterns of Drp1 in GABAergic neurons. We also further analyzed Drp1 expression in human malignant glioma tissue. Results : Drp1 was widely but heterogeneously distributed in the central nervous system. Further observation indicated that Drp1 was highly and heterogeneously expressed in inhibitory neurons. Under transmission electron microscopy, the distribution of Drp1 was higher in dendrites than other areas in neurons, and only a small amount of Drp1 was localized in mitochondria. In human malignant glioma, the fluorescence intensity of Drp1 increased from grade I-III, while grade IV showed a declining trend. Conclusion: In this study, we observed a wide heterogeneous distribution of Drp1 in the central nervous system, which might be related to the occurrence and development of neurologic disease. We hope that the relationship between Drp1 and mitochondria may will to therapeutic guidance in the clinic.

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