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.

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 Behaviour of oligodendrocytes and Schwann cells in an experimental model of toxic demyelination of the central nervous system

2001 ◽  
Vol 59 (2B) ◽  
pp. 358-361 ◽  
Author(s):  
Dominguita Lühers Graça ◽  
Eduardo Fernandes Bondan ◽  
Luis Antonio Violin Dias Pereira ◽  
Cristina Gevehr Fernandes ◽  
Paulo César Maiorka
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Schwann Cells ◽  
Experimental Model ◽  
Glial Cells ◽  
Ethidium Bromide ◽  
Wistar Rats ◽  
Myelin Sheaths ◽  
Complex Processes ◽  
The Central Nervous System

Oligodendrocytes and Schwann cells are engaged in myelin production, maintenance and repairing respectively in the central nervous system (CNS) and the peripheral nervous system (PNS). Whereas oligodendrocytes act only within the CNS, Schwann cells are able to invade the CNS in order to make new myelin sheaths around demyelinated axons. Both cells have some limitations in their activities, i.e. oligodendrocytes are post-mitotic cells and Schwann cells only get into the CNS in the absence of astrocytes. Ethidium bromide (EB) is a gliotoxic chemical that when injected locally within the CNS, induce demyelination. In the EB model of demyelination, glial cells are destroyed early after intoxication and Schwann cells are free to approach the naked central axons. In normal Wistar rats, regeneration of lost myelin sheaths can be achieved as early as thirteen days after intoxication; in Wistar rats immunosuppressed with cyclophosphamide the process is delayed and in rats administered cyclosporine it may be accelerated. Aiming the enlightening of those complex processes, all events concerning the myelinating cells in an experimental model are herein presented and discussed.

scholarly journals Axonal mitochondria across species adjust in diameter depending on thickness of surrounding myelin

2019 ◽  
Author(s):  
Benjamin V Ineichen ◽  
Keying Zhu ◽  
Karl E Carlström
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Experimental Models ◽  
Metabolic Status ◽  
Myelinated Axons ◽  
Myelin Sheaths ◽  
Pathological Conditions ◽  
The Central Nervous System ◽  
Myelin Thickness

AbstractIn the central nervous system (CNS), axons and its surrounding myelin sheaths, generated by oligodendrocytes, greatly depend on each other, where oligodendrocytes provide axons with both trophic and metabolic support. Across spices, assessment of the axon-myelin ultrastructure is the key-approach to visualize de- and re-myelination of axons. However, this assessment omits to provide information on axonal homeostasis or how axon-myelin influence one another. Since mitochondria may adjust in size thus mirroring the intracellular physiological and metabolic status we applied this to myelinated axons in the CNS. We herein show that a large axonal mitochondria diameter correlates with thinner surrounding myelin sheaths across different CNS tracts and species, including human. We also show that the relation between axonal mitochondria diameter and surrounding myelin thickness is a valuable measurement to verify advanced remyelination in two commonly used experimental demyelinating models, namely the cuprizone and the lysolecithin (LPC) model. Lastly, we show that axonal mitochondria adjust in diameter in response to the thickness of the axonal surrounding myelin whereas the opposite adaption was absent. In summary, the link between axonal mitochondria diameter and surrounding myelin thickness provide insight on the axon-myelin relation both during homeostasis and pathological conditions. This link is also translational applicable and can thus contribute to a better understanding on how to study remyelination using experimental models.

scholarly journals Acute Disseminated Encephalomyelitis (ADEM): A Demyelinating Disease with Specific Morphological Features

2021 ◽  
pp. 106689692199356
Author(s):  
Fleur Cordier ◽  
Lars Velthof ◽  
David Creytens ◽  
Jo Van Dorpe
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Differential Diagnosis ◽  
Clinical Case ◽  
Demyelinating Disease ◽  
Acute Disseminated Encephalomyelitis ◽  
Demyelinating Diseases ◽  
Demyelinating Disorder ◽  
Immune Mediated ◽  
The Central Nervous System

Acute disseminated encephalomyelitis (ADEM) is a rare immune-mediated inflammatory and demyelinating disorder of the central nervous system. Its characteristic perivenular demyelination and inflammation aid in the differential diagnosis with other inflammatory demyelinating diseases. Here, we present a clinical case of ADEM, summarize its histological hallmarks, and discuss pitfalls concerning the most important neuropathological differential diagnoses.

scholarly journals The nervous form of canine distemper

2018 ◽  
Vol 13 (2) ◽  
pp. 125-136
Author(s):  
Alice Fernandes Alfieri ◽  
Alexandre Mendes Amude ◽  
Amauri Alcindo Alfier
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Canine Distemper Virus ◽  
Demyelinating Disease ◽  
Clinical Course ◽  
Systemic Infection ◽  
Canine Distemper ◽  
Systemic Involvement ◽  
Clinical Syndromes ◽  
The Central Nervous System

Canine distemper is a systemic infection, frequently lethal in dogs. The canine distemper virus(CDV) causes a persistent infection within the central nervous system resulting in aprogressive, multifocal demyelinating disease. In dogs, CDV infection may lead togastrointestinal and/or respiratory signs, frequently with central nervous system involvement.Myoclonus has been a common and characteristic sign observed in dogs with distemperencephalomyelitis. However, the nervous form of distemper may occur in the absence ofmyoclonus and systemic involvement. This review will point the clinical course and theneurological signs of nervous distemper, as well the clinical syndromes of CDV infection,neuropathology of acute and chronic demyelination, and diagnostic aids of CDVencephalomyelitis.

scholarly journals Schwannoma of the arythenoid

2013 ◽  
Vol 11 (2) ◽  
pp. 224-226 ◽  
Author(s):  
Carlos Eduardo Molinari Nardi ◽  
Alexandre Wakil Burzichelli ◽  
Elio Gilberto Pfuetzenreiter ◽  
Rogerio Aparecido Dedivitis
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Schwann Cells ◽  
Rare Case ◽  
Nerve Fibers ◽  
Endoscopic Procedure ◽  
The Central Nervous System

Schwannoma is a benign encapsulated tumor that originates from the Schwann cells lining nerve fibers outside the central nervous system. We report a rare case of schwannoma that arose from the left arythenoid cartilage The patient underwent excision of the mass through microlaryngeal endoscopic procedure. No recurrence was observed during follow-up.

scholarly journals Acute Disseminated Encephalomyelitis Following Typhoid Fever: A Case Report

2014 ◽  
Vol 9 (4) ◽  
pp. 55-58
Author(s):  
R Adhikari ◽  
A Tayal ◽  
PK Chhetri ◽  
B Pokhrel
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Case Report ◽  
Typhoid Fever ◽  
Demyelinating Disease ◽  
Acute Disseminated Encephalomyelitis ◽  
Medical Sciences ◽  
Cerebellar Syndrome ◽  
Immune Mediated ◽  
The Central Nervous System

The involvement of central nervous system in children with typhoid fever is common. Acute disseminated encephalomyelitis is a rare immune mediated and demyelinating disease of the central nervous system that usually affects children. We report a 7-year-old child with typhoid fever who developed acute cerebellar syndrome due to acute disseminated encephalomyelitis.Journal of College of Medical Sciences-Nepal, 2013, Vol-9, No-4, 55-58 DOI: http://dx.doi.org/10.3126/jcmsn.v9i4.10237

A Diagnostic Pointer to Adult Metachromatic Leucodystrophy

1980 ◽  
Vol 137 (2) ◽  
pp. 186-187 ◽  
Author(s):  
John A. O. Besson
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Autosomal Recessive ◽  
Demyelinating Disease ◽  
Initial Manifestation ◽  
The Central Nervous System ◽  
Metachromatic Leucodystrophy ◽  
Arylsulphatase A ◽  
Recessive Defect

Adult metachromatic leucodystrophy (MLD) is a rare demyelinating disease of the central nervous system caused by a genetic autosomal recessive defect and mediated through a deficiency in the enzyme arylsulphatase A (Peiffer, 1970). The initial manifestation may take the form of symptoms suggestive of schizophrenia or dementia (Sourander et al, 1962; Austin et al, 1968).

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