scholarly journals Eag1 K+Channel: Endogenous Regulation and Functions in Nervous System

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Bo Han ◽  
Tursonjan Tokay ◽  
Guangming Zhang ◽  
Peng Sun ◽  
Shangwei Hou

Ether-à-go-go1 (Eag1, Kv10.1, KCNH1) K+channel is a member of the voltage-gated K+channel family mainly distributed in the central nervous system and cancer cells. Like other types of voltage-gated K+channels, the EAG1 channels are regulated by a variety of endogenous signals including reactive oxygen species, rendering the EAG1 to be in the redox-regulated ion channel family. The role of EAG1 channels in tumor development and its therapeutic significance have been well established. Meanwhile, the importance of hEAG1 channels in the nervous system is now increasingly appreciated. The present review will focus on the recent progress on the channel regulation by endogenous signals and the potential functions of EAG1 channels in normal neuronal signaling as well as neurological diseases.

2021 ◽  
Vol 13 ◽  
Author(s):  
Banglian Hu ◽  
Shengshun Duan ◽  
Ziwei Wang ◽  
Xin Li ◽  
Yuhang Zhou ◽  
...  

The colony-stimulating factor 1 receptor (CSF1R) is a key tyrosine kinase transmembrane receptor modulating microglial homeostasis, neurogenesis, and neuronal survival in the central nervous system (CNS). CSF1R, which can be proteolytically cleaved into a soluble ectodomain and an intracellular protein fragment, supports the survival of myeloid cells upon activation by two ligands, colony stimulating factor 1 and interleukin 34. CSF1R loss-of-function mutations are the major cause of adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) and its dysfunction has also been implicated in other neurodegenerative disorders including Alzheimer’s disease (AD). Here, we review the physiological functions of CSF1R in the CNS and its pathological effects in neurological disorders including ALSP, AD, frontotemporal dementia and multiple sclerosis. Understanding the pathophysiology of CSF1R is critical for developing targeted therapies for related neurological diseases.


2010 ◽  
Vol 21 (5-6) ◽  
pp. 394-408 ◽  
Author(s):  
Cláudia P. Figueiredo ◽  
Fabrício A. Pamplona ◽  
Tânia L. Mazzuco ◽  
Aderbal S. Aguiar ◽  
Roger Walz ◽  
...  

Antioxidants ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 216 ◽  
Author(s):  
Marika Cordaro ◽  
Salvatore Cuzzocrea ◽  
Rosalia Crupi

The inflammation process represents of a dynamic series of phenomena that manifest themselves with an intense vascular reaction. Neuroinflammation is a reply from the central nervous system (CNS) and the peripheral nervous system (PNS) to a changed homeostasis. There are two cell systems that mediate this process: the glia of the CNS and the lymphocites, monocytes, and macrophages of the hematopoietic system. In both the peripheral and central nervous systems, neuroinflammation plays an important role in the pathogenesis of neurodegenerative diseases, such as Parkinson’s and Alzheimer’s diseases, and in neuropsychiatric illnesses, such as depression and autism spectrum disorders. The resolution of neuroinflammation is a process that allows for inflamed tissues to return to homeostasis. In this process the important players are represented by lipid mediators. Among the naturally occurring lipid signaling molecules, a prominent role is played by the N-acylethanolamines, namely N-arachidonoylethanolamine and its congener N-palmitoylethanolamine, which is also named palmitoylethanolamide or PEA. PEA possesses a powerful neuroprotective and anti-inflammatory power but has no antioxidant effects per se. For this reason, its co-ultramicronization with the flavonoid luteolin is more efficacious than either molecule alone. Inhibiting or modulating the enzymatic breakdown of PEA represents a complementary therapeutic approach to treating neuroinflammation. The aim of this review is to discuss the role of ultramicronized PEA and co-ultramicronized PEA with luteolin in several neurological diseases using preclinical and clinical approaches.


2020 ◽  
Vol 18 (9) ◽  
pp. 861-867
Author(s):  
Kai Chen ◽  
Liu Nan Yang ◽  
Chuan Lai ◽  
Dan Liu ◽  
Ling-Qiang Zhu

Glutamate receptor, ionotropic, N-methyl-D-aspartate associated protein 1 (GRINA) is a member of the NMDA receptors (NMDARs) and is involved in several neurological diseases, which governs the key processes of neuronal cell death or the release of neurotransmitters. Upregulation of GRINA has been reported in multiple diseases in human beings, such as major depressive disorder (MDD) and schizophrenia (SCZ), with which the underlying mechanisms remain elusive. In this review, we provide a general overview of the expression and physiological function of GRINA in the central nervous system (CNS) diseases, including stroke, depression ,epilepsy, SCZ, and Alzheimer’s disease (AD).


2021 ◽  
Vol 12 ◽  
Author(s):  
Xinyi Wang ◽  
Zhe Hu ◽  
Kai Zhong

Epilepsy, which is characterized by spontaneous recurrent seizures, is one of the most common and serious chronic neurological diseases in the world. 30% patients failed to control seizures with multiple anti-seizure epileptic drugs, leading to serious outcomes. The pathogenesis of epilepsy is very complex and remains unclear. Brain-derived neurotrophic factor (BDNF), as a member of the neurotrophic factor family, is considered to play an important role in the survival, growth and differentiation of neurons during the development of the central nervous system. Recent years, a series of studies have reported that BDNF can maintain the function of the nervous system and promotes the regeneration of neurons after injury, which is believed to be closely related to epileptogenesis. However, two controversial views (BDNF inhibits or promotes epileptogenesis) still exist. Thus, this mini-review focuses on updating the new evidence of the role of BDNF in epileptogenesis and discussing the possibility of BDNF as an underlying target for the treatment of epilepsy.


2020 ◽  
pp. 49-56
Author(s):  
T. Shirshova

Disorders of the musculoskeletal system in school-age children occupy 1-2 places in the structure of functional abnormalities. Cognitive impairment without organic damage to the central nervous system is detected in 30-56% of healthy school children. Along with the increase in the incidence rate, the demand for rehabilitation systems, which allow patients to return to normal life as soon as possible and maintain the motivation for the rehabilitation process, is also growing. Adaptation of rehabilitation techniques, ease of equipment management, availability of specially trained personnel and availability of technical support for complexes becomes important.


Author(s):  
Konstantin Gulyabin

Mills' syndrome is a rare neurological disorder. Its nosological nature is currently not completely determined. Nevertheless, Mills' syndrome is considered to be a rare variant of the degenerative pathology of the central nervous system – a variant of focal cortical atrophy. The true prevalence of this pathology is unknown, since this condition is more often of a syndrome type, observed in the clinical picture of a number of neurological diseases (primary lateral sclerosis, frontotemporal dementia, etc.) and is less common in isolated form.


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