Acetylcholinesterase Inhibitors for Alzheimer’s disease: Past, Present, and Potential Future

2020 ◽  
Vol 8 (12) ◽  
Author(s):  
Brandon Truong ◽  
Jose Quiroz ◽  
Ronny Priefer
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cognitive Decline ◽  
Neurodegenerative Disorder ◽  
Neuronal Damage ◽  
Neuronal Loss ◽  
Acetylcholinesterase Inhibitors ◽  
Cognitive Symptoms ◽  
The Past ◽  
The Central Nervous System

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.

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 ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurodegenerative Disorders ◽  
Crucial Role ◽  
Microglial Activation ◽  
Neuronal Damage ◽  
Therapeutic Targets ◽  
Neuroprotective Activity ◽  
The Past ◽  
The Central Nervous System

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.

scholarly journals Vesicular dysfunction and pathways to neurodegeneration

2021 ◽  
Author(s):  
Patrick A. Lewis
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Human Brain ◽  
Cell Viability ◽  
Case Studies ◽  
Neurological Diseases ◽  
The Past ◽  
Cellular Events ◽  
The Central Nervous System ◽  
Cellular Control

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.

Diseases of the central nervous system after malaria

2021 ◽  
Vol 20 (5) ◽  
pp. 500-508
Author(s):  
G. V. Pervushin
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
The Past ◽  
The Central Nervous System

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

scholarly journals Adiponectin and Cognitive Decline

2020 ◽  
Vol 21 (6) ◽  
pp. 2010 ◽  
Author(s):  
Maria Rosaria Rizzo ◽  
Renata Fasano ◽  
Giuseppe Paolisso
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cognitive Decline ◽  
Neural Plasticity ◽  
Verbal Memory ◽  
Main Role ◽  
Menopausal Women ◽  
The Central Nervous System ◽  
The Relationship ◽  
The Brain

Adiponectin (ADPN) is a plasma protein secreted by adipose tissue showing pleiotropic effects with anti-diabetic, anti-atherogenic, and anti-inflammatory properties. Initially, it was thought that the main role was only the metabolism control. Later, ADPN receptors were also found in the central nervous system (CNS). In fact, the receptors AdipoR1 and AdipoR2 are expressed in various areas of the brain, including the hypothalamus, hippocampus, and cortex. While AdipoR1 regulates insulin sensitivity through the activation of the AMP-activated protein kinase (AMPK) pathway, AdipoR2 stimulates the neural plasticity through the activation of the peroxisome proliferator-activated receptor alpha (PPARα) pathway that inhibits inflammation and oxidative stress. Overall, based on its central and peripheral actions, ADPN appears to have neuroprotective effects by reducing inflammatory markers, such as C-reactive protein (PCR), interleukin 6 (IL6), and Tumor Necrosis Factor a (TNFa). Conversely, high levels of inflammatory cascade factors appear to inhibit the production of ADPN, suggesting bidirectional modulation. In addition, ADPN appears to have insulin-sensitizing action. It is known that a reduction in insulin signaling is associated with cognitive impairment. Based on this, it is of great interest to investigate the mechanism of restoration of the insulin signal in the brain as an action of ADPN, because it is useful for testing a possible pharmacological treatment for the improvement of cognitive decline. Anyway, if ADPN regulates neuronal functioning and cognitive performances by the glycemic metabolic system remains poorly explored. Moreover, although the mechanism is still unclear, women compared to men have a doubled risk of developing cognitive decline. Several studies have also supported that during the menopausal transition, the estrogen reduction can adversely affect the brain, in particular, verbal memory and verbal fluency. During the postmenopausal period, in obese and insulin-resistant individuals, ADPN serum levels are significantly reduced. Our recent study has evaluated the relationship between plasma ADPN levels and cognitive performances in menopausal women. Thus, the aim of this review is to summarize both the mechanisms and the effects of ADPN in the central nervous system and the relationship between plasma ADPN levels and cognitive performances, also in menopausal women.

Central Nervous System Processing of Human Visceral Pain in Health and Disease

Physiology ◽  
2003 ◽  
Vol 18 (3) ◽  
pp. 109-114 ◽  
Author(s):  
Anthony R. Hobson ◽  
Qasim Aziz
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Visceral Pain ◽  
Functional Gastrointestinal Disorders ◽  
Functional Brain Imaging ◽  
Gastrointestinal Disorders ◽  
The Past ◽  
Body Of Knowledge ◽  
The Central Nervous System ◽  
Health And Disease

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.

scholarly journals p53 induction is associated with neuronal damage in the central nervous system.

1994 ◽  
Vol 91 (16) ◽  
pp. 7525-7529 ◽  
Author(s):  
S. Sakhi ◽  
A. Bruce ◽  
N. Sun ◽  
G. Tocco ◽  
M. Baudry ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neuronal Damage ◽  
The Central Nervous System

scholarly journals Uncovering Novel Roles of Nonneuronal Cells in Body Weight Homeostasis and Obesity

Endocrinology ◽  
2013 ◽  
Vol 154 (9) ◽  
pp. 3001-3007 ◽  
Author(s):  
Julie A. Chowen ◽  
Jesús Argente ◽  
Tamas L. Horvath
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Glial Cells ◽  
Secondary Complications ◽  
Physiological Regulation ◽  
Structural Support ◽  
The Past ◽  
The Central Nervous System ◽  
Poor Nutrition ◽  
Heterogeneous Class

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.

scholarly journals Chemokines Referee Inflammation within the Central Nervous System during Infection and Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Douglas M. Durrant ◽  
Jessica L. Williams ◽  
Brian P. Daniels ◽  
Robyn S. Klein
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Essential Role ◽  
Inflammatory Cell ◽  
Cell Types ◽  
Effector Molecules ◽  
The Past ◽  
Inflammatory Conditions ◽  
Endothelial Barriers ◽  
The Central Nervous System

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.

Sign in / Sign up

Export Citation Format

Share Document