scholarly journals A New Rise of Non-Human Primate Models of Synucleinopathies

Biomedicines ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 272
Author(s):  
Margaux Teil ◽  
Marie-Laure Arotcarena ◽  
Benjamin Dehay
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurodegenerative Diseases ◽  
Translational Research ◽  
Experimental Models ◽  
Preclinical Model ◽  
Key Characteristics ◽  
Intracytoplasmic Inclusions ◽  
The Central Nervous System ◽  
Human Primate

Synucleinopathies are neurodegenerative diseases characterized by the presence of α-synuclein-positive intracytoplasmic inclusions in the central nervous system. Multiple experimental models have been extensively used to understand better the mechanisms involved in the pathogenesis of synucleinopathy. Non-human primate (NHP) models are of interest in neurodegenerative diseases as they constitute the highest relevant preclinical model in translational research. They also contribute to bringing new insights into synucleinopathy’s pathogenicity and help in the quest and validation of therapeutical strategies. Here, we reviewed the different NHP models that have recapitulated key characteristics of synucleinopathy, and we aimed to highlight the contribution of NHP in mechanistic and translational approaches for synucleinopathies.

Schwann cell transplantation and myelin repair of the CNS

1997 ◽  
Vol 3 (2) ◽  
pp. 157-161 ◽  
Author(s):  
A. Baron-Van Evercooren ◽  
V. Avellana-Adalid ◽  
F. Lachapelle ◽  
R. Liblau
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Schwann Cell ◽  
Schwann Cells ◽  
Cell Transplantation ◽  
Autologous Transplantation ◽  
Experimental Models ◽  
Primate Model ◽  
The Central Nervous System ◽  
Human Primate

Studies with experimental models of dysmyelination and demyelination have shown that rodent Schwann cells including a Schwann cell line, transplanted in the central nervous system compete with host oligodendrocytes to remyelinate denuded central axons of the spinal cord. The myelin produced by transplanted SC around these central nervous system axons is structurally normal and restores, secure nerve conduction. In the presence of a favorable substrate, transplanted Schwann cells migrate over considerable distances (several mm) and are recruited by a demyelinated lesion which they will partially repair. Thus Schwann cells, which can also support axonal growth, may be instrumental in central nervous system repair. In addition, the possibility of obtaining large quantities of human and non-human primate Schwann cells, makes it possible to consider autologous Schwann cell transplantation as a potential therapy for demyelinating or traumatic diseases. The various differences which may exist between rodents and humans, however, require further investigation of this possibility in a non-human primate model of demyelination. These experiments should provide not only insights on the potential of autologous transplantation in primates but also a better understanding of the process of central remyelination.

scholarly journals Biology of the repair of central nervous system demyelinated lesions: an appraisal

1996 ◽  
Vol 54 (2) ◽  
pp. 331-334 ◽  
Author(s):  
L. A. V Peireira ◽  
M. A. Cruz-Höfling ◽  
M. S. J. Dertkigil ◽  
D. L. Graça
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Schwann Cells ◽  
Demyelinating Disease ◽  
Experimental Models ◽  
Primitive Cell ◽  
Marked Influence ◽  
Myelin Sheaths ◽  
Human Material ◽  
The Central Nervous System

The integrity of myelin sheaths is maintained by oligodendrocytes and Schwann cells respectively in the central nervous system (CNS) and in the peripheral nervous system. The process of demyelination consisting of the withdrawal of myelin sheaths from their axons is a characteristic feature of multiple sclerosis, the most common human demyelinating disease. Many experimental models have been designed to study the biology of demyelination and remyelination (repair of the lost myelin) in the CNS, due to the difficulties in studying human material. In the ethidium bromide (an intercalating gliotoxic drug) model of demyelination, CNS remyelination may be carried out by surviving oligodendrocytes and/or by cells differentiated from the primitive cell lines or either by Schwann cells that invade the CNS. However, some factors such as the age of the experimental animals, intensity and time of exposure to the intercalating chemical and the topography of the lesions have marked influence on the repair of the tissue.

scholarly journals Central Nervous System Cell-Derived Exosomes in Neurodegenerative Diseases

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Yang Tian ◽  
Chen Fu ◽  
Yifan Wu ◽  
Yao Lu ◽  
Xuemei Liu ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurodegenerative Diseases ◽  
Extracellular Vesicles ◽  
Mammalian Cells ◽  
Glia Cells ◽  
Central Nervous System Cell ◽  
The Central Nervous System ◽  
System Cell ◽  
Almost All

Exosomes are a type of extracellular vesicles secreted by almost all kinds of mammalian cells that shuttle “cargo” from one cell to another, indicative of its role in cell-to-cell transportation. Interestingly, exosomes are known to undergo alterations or serve as a pathway in multiple diseases, including neurodegenerative diseases. In the central nervous system (CNS), exosomes originating from neurons or glia cells contribute to or inhibit the progression of CNS-related diseases in special ways. In lieu of this, the current study investigated the effect of CNS cell-derived exosomes on different neurodegenerative diseases.

scholarly journals Effect of Luteolin and Apigenin on the Production of Il-31 and Il-33 in Lipopolysaccharides-Activated Microglia Cells and Their Mechanism of Action

Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 811 ◽  
Author(s):  
Denis Nchang Che ◽  
Byoung Ok Cho ◽  
Ji-su Kim ◽  
Jae Young Shin ◽  
Hyun Ju Kang ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurodegenerative Diseases ◽  
Signaling Pathways ◽  
Nuclear Translocation ◽  
Mapk Pathway ◽  
Microglial Cells ◽  
Stat3 Signaling ◽  
Protein Expressions ◽  
The Central Nervous System

Microglia cells are resident cells of the central nervous system (CNS) charged with modulating inflammation in the CNS. Overstimulation of microglia cells continuously releases inflammatory mediators that contribute to neurodegenerative diseases. Apigenin and Luteolin are flavonoids with reported anti-inflammatory activities. However, their effects on IL-31 and IL-33 production in microglial cells are unknown. Here, we investigated the effects of apigenin and luteolin on the production of IL-31 and IL-33 by microglia cells. SIM-A9 microglial cells were pre-treated with apigenin or luteolin and stimulated with lipopolysaccharides to evaluate the production of IL-31 and IL-33. The study revealed that apigenin and luteolin inhibited the production of IL-31 and IL-33 at the gene and protein expressions and the secretion levels. Using potent inhibitors of MAPK, NF-κB, and STAT3 signaling pathways, we demonstrated that apigenin and luteolin’s suppression of ERK and JNK contributed to the inhibition of IL-31 and IL-33 in the MAPK pathway. Luteolin’s suppression of NF-κB and STAT3 also contributed to the inhibition of IL-31 and IL-33. Further analysis revealed that both compounds prevented nuclear translocation of activated NF-κB and STAT3, an act that subsequently prevented their DNA binding activities. Collectively, the study suggested that apigenin and luteolin’s regulation of signaling pathways contributed to the inhibition of IL-31 and IL-33, thus suggesting its importance for the improvement of neurodegenerative diseases involving these two cytokines.

scholarly journals The Role of Metals in Neurodegenerative Diseases of the Central Nervous System

2020 ◽  
Vol 8 (2) ◽  
pp. 130-146
Author(s):  
Afshin Montazeri ◽  
Milad Akhlaghi ◽  
Ahmad Reza Barahimi ◽  
Ali Jahanbazi Jahan Abad ◽  
Reza Jabbari ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurodegenerative Diseases ◽  
The Central Nervous System

scholarly journals Current Understanding of Central Nervous System Drainage Systems: Implications in the Context of Neurodegenerative Diseases

2020 ◽  
Vol 18 (11) ◽  
pp. 1054-1063 ◽  
Author(s):  
Vladimir N. Nikolenko ◽  
Marine V. Oganesyan ◽  
Angela D. Vovkogon ◽  
Arina T. Nikitina ◽  
Ekaterina A. Sozonova ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurodegenerative Diseases ◽  
Lymphatic Vessels ◽  
Basal Area ◽  
Waste Products ◽  
Glymphatic System ◽  
The Central Nervous System ◽  
New Perspective ◽  
And Function

Until recently, it was thought that there were no lymphatic vessels in the central nervous system (CNS). Therefore, all metabolic processes were assumed to take place only in the circulation of the cerebrospinal fluid (CSF) and through the blood-brain barrier’s (BBB), which regulate ion transport and ensure the functioning of the CNS. However, recent findings yield a new perspective: There is an exchange of CSF with interstitial fluid (ISF), which is drained to the paravenous space and reaches lymphatic nodes at the end. This circulation is known as the glymphatic system. The glymphatic system is an extensive network of meningeal lymphatic vessels (MLV) in the basal area of the skull that provides another path for waste products from CNS to reach the bloodstream. MLV develop postnatally, initially appearing around the foramina in the basal part of the skull and the spinal cord, thereafter sprouting along the skull’s blood vessels and spinal nerves in various areas of the meninges. VEGF-C protein (vascular endothelial growth factor), expressed mainly by vascular smooth cells, plays an important role in the development of the MLV. The regenerative potential and plasticity of MLV and the novel discoveries related to CNS drainage offer potential for the treatment of neurodegenerative diseases such as dementia, hydrocephalus, stroke, multiple sclerosis, and Alzheimer disease (AD). Herein, we present an overview of the structure and function of the glymphatic system and MLV, and their potential involvement in the pathology and progression of neurodegenerative diseases.

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