scholarly journals Herbal Compounds Play a Role in Neuroprotection through the Inhibition of Microglial Activation

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Yan Fu ◽  
Jianmei Yang ◽  
Xingyu Wang ◽  
Pin Yang ◽  
Yang Zhao ◽  
...  

Since microglia possess both neuroprotective and neurotoxic potential, they play a crucial role in the central nervous system (CNS). Excessive microglial activation induces inflammation-mediated neuronal damage and degeneration. At present, numerous herbal compounds are able to suppress neurotoxicity via inhibiting microglial activation. Therefore, many researchers focus on pharmacological inhibitors of microglial activation to ameliorate neurodegenerative disorders. Further work should concentrate on the exploration of new herbal compounds, which characteristically inhibit microglial neurotoxicity, rather than modulating neuroprotection alone. In this review, we summarize these herbal compounds, which in the past several years have been shown to exert potential neuroprotective activity by inhibiting microglial activation. The therapeutic targets and pharmacological mechanisms of these compounds have also been discussed.

2020 ◽  
Vol 8 (12) ◽  
Author(s):  
Brandon Truong ◽  
Jose Quiroz ◽  
Ronny Priefer

Alzheimer’s Diseases (AD) is a neurodegenerative disorder characterized by progressive neuronal loss leading to cognitive decline. Although there is yet to be a cure nor a way to reverse the neuronal damage, there are current treatments to amend some of the cognitive symptoms associated with AD. Acetylcholinesterase inhibitors (AChEi) are the primary agents of choice and have had profound implications throughout the past decades. AChEi such as donepezil, rivastigmine, and galantamine mediates and increases cholinergic activities in the central nervous system (CNS), and have been shown to improve and preserve cognition in AD patients. Beyond the current drugs on the market, investigational discoveries continue to explore the potential of safer and more efficacious AChEi agents for the treatment of AD. There have been quite a few challenges, given the high failure rates. Yet, these very trials and studies have been a fundamental step towards better understanding the treatments of AD and have provided some insight on the potential to surpass what is currently available.


2021 ◽  
Author(s):  
Patrick A. Lewis

Abstract Cellular control of vesicle biology and trafficking is critical for cell viability, with disruption of these pathways within the cells of the central nervous system resulting in neurodegeneration and disease. The past two decades have provided important insights into both the genetic and biological links between vesicle trafficking and neurodegeneration. In this essay, the pathways that have emerged as being critical for neuronal survival in the human brain will be discussed – illustrating the diversity of proteins and cellular events with three molecular case studies drawn from different neurological diseases.


2016 ◽  
Vol 138 (5) ◽  
pp. 653-693 ◽  
Author(s):  
Katrin I. Andreasson ◽  
Adam D. Bachstetter ◽  
Marco Colonna ◽  
Florent Ginhoux ◽  
Clive Holmes ◽  
...  

2021 ◽  
Vol 20 (5) ◽  
pp. 500-508
Author(s):  
G. V. Pervushin

Despite the enormous incidence of malaria over the past 2 years, complications of this disease from the nervous system are relatively rare.


Physiology ◽  
2000 ◽  
Vol 15 (5) ◽  
pp. 250-255
Author(s):  
Michael A. Klein ◽  
Adriano Aguzzi

Prion diseases are fatal neurodegenerative disorders of animals and humans. Here we address the role of the immune system in the spread of prions from peripheral sites to the central nervous system and its potential relevance to iatrogenic prion disease.


Physiology ◽  
2003 ◽  
Vol 18 (3) ◽  
pp. 109-114 ◽  
Author(s):  
Anthony R. Hobson ◽  
Qasim Aziz

To understand the pathophysiology of anomalous pain in functional gastrointestinal disorders, we must increase our understanding of how the central nervous system processes visceral pain. Over the past decade, novel application of functional brain imaging and electrophysiological techniques has given us the opportunity to study these processes in humans, and this review summarizes the current body of knowledge.


1994 ◽  
Vol 91 (16) ◽  
pp. 7525-7529 ◽  
Author(s):  
S. Sakhi ◽  
A. Bruce ◽  
N. Sun ◽  
G. Tocco ◽  
M. Baudry ◽  
...  

Endocrinology ◽  
2013 ◽  
Vol 154 (9) ◽  
pp. 3001-3007 ◽  
Author(s):  
Julie A. Chowen ◽  
Jesús Argente ◽  
Tamas L. Horvath

Glial cells, which constitute more than 50% of the mass of the central nervous system and greatly outnumber neurons, are at the vanguard of neuroendocrine research in metabolic control and obesity. Historically relegated to roles of structural support and protection, diverse functions have been gradually attributed to this heterogeneous class of cells with their protagonism in crescendo in all areas of neuroscience during the past decade. However, this dramatic increase in attention bestowed upon glial cells has also emphasized our vast lack of knowledge concerning many aspects of their physiological functions, let alone their participation in numerous pathologies. This minireview focuses on the recent advances in our understanding of how glial cells participate in the physiological regulation of appetite and systemic metabolism as well as their role in the pathophysiological response to poor nutrition and secondary complications associated with obesity. Moreover, we highlight some of the existing lagoons of knowledge in this increasingly important area of investigation.


2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Douglas M. Durrant ◽  
Jessica L. Williams ◽  
Brian P. Daniels ◽  
Robyn S. Klein

The discovery that chemokines and their receptors are expressed by a variety of cell types within the normal adult central nervous system (CNS) has led to an expansion of their repertoire as molecular interfaces between the immune and nervous systems. Thus, CNS chemokines are now divided into those molecules that regulate inflammatory cell migration into the CNS and those that initiate CNS repair from inflammation-mediated tissue damage. Work in our laboratory throughout the past decade has sought to elucidate how chemokines coordinate leukocyte entry and interactions at CNS endothelial barriers, under both homeostatic and inflammatory conditions, and how they promote repair within the CNS parenchyma. These studies have identified several chemokines, including CXCL12 and CXCL10, as critical regulators of leukocyte migration from perivascular locations. CXCL12 additionally plays an essential role in promoting remyelination of injured white matter. In both scenarios we have shown that chemokines serve as molecular links between inflammatory mediators and other effector molecules involved in neuroprotective processes.


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