About: Inside-Out versus Outside-In models for virus induced demyelination: axonal damage triggering demyelination

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About: Inside-Out versus Outside-In models for virus induced demyelination: axonal damage triggering demyelination Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Inside-Out versus Outside-In models for virus induced demyelination: axonal damage triggering demyelination
Creator	Tsunoda, Ikuo Fujinami, Robert
source	Medline; PMC
abstract	The primary target in multiple sclerosis (MS) is believed to be either myelin itself (myelinopathy) or the myelin-forming cell, the oligodendrocyte (oligodendrogliopathy). Although axonal injury occurs in MS, it is regarded as a secondary event to the myelin damage. Here, the lesion develops from myelin (outside) to the axon (inside) (Outside-In model). Recently, gray matter lesions and axonal injury in normal-appearing white matter have also been reported in MS. This raises two questions. 1) Is axonal injury exclusively secondary to myelin damage or from a direct insult to the axon or neurons (axonopathy)? (2) Is the injured axon regarded as only an end result of pathology or disease, or can axonal injury contribute to the spread of secondary damage, including demyelination? The former is raised from the fact that axonal damage has been reported in several virus infections, including human immunodeficiency virus, human T-lymphotropic virus 1, herpes simplex virus and coronavirus, which also cause demyelination. The latter possibility where axonal injury leads to other changes is raised from the rather unexpected similarity between spinal cord injury (SCI) and MS where axonal injury, oligodendrocyte apoptosis and demyelination are all present. In SCI, transection of axons leads to delayed oligodendrocyte apoptosis with secondary demyelination. Neurofilament immunostaining of spinal cord sections demonstrates that axonal injury with oligodendrocyte apoptosis also precedes demyelination in an animal model for MS, Theiler’s murine encephalomyelitis virus infection. This implies that axonal injury could trigger demyelination. In this instance, lesions develop from the axon (inside) to the myelin (outside) (Inside-Out model).
has issue date	2002-01-01(xsd:dateTime)
bibo:doi	10.1007/s00281-002-0105-z
bibo:pmid	12503060
has license	no-cc
sha1sum (hex)	4582ac8e28c6b824d39fad57b7d70cff2fd44971
schema:url	https://doi.org/10.1007/s00281-002-0105-z
resource representing a document's title	Inside-Out versus Outside-In models for virus induced demyelination: axonal damage triggering demyelination
has PubMed Central identifier	PMC7079941
has PubMed identifier	12503060
schema:publication	Springer Semin Immunopathol
resource representing a document's body	covid:4582ac8e28c6b824d39fad57b7d70cff2fd44971#body_text
is schema:about of	named entity 'MODELS' named entity 'damage' named entity 'model' named entity 'implies' named entity 'axon' named entity 'axons' named entity 'lesions' named entity 'MURINE ENCEPHALOMYELITIS VIRUS' named entity 'DELAYED' named entity 'AXONAL DAMAGE' named entity 'NEURONS' named entity 'SECONDARY TO' named entity 'CHANGES' named entity 'OUTSIDE' named entity 'SPINAL CORD INJURY' named entity 'HUMAN IMMUNODEFICIENCY VIRUS' named entity 'VIRUS INFECTION' named entity 'OLIGODENDROCYTE APOPTOSIS' named entity 'TARGET' named entity 'LESIONS' named entity 'INJURED' named entity 'REPORTED' named entity 'NEUROFILAMENT' named entity 'PRIMARY' named entity 'CORONAVIRUS' named entity 'DISEASE' named entity 'AXONAL INJURY' named entity 'LEADS' named entity 'INCLUDING' named entity 'AXON' named entity 'IMMUNOSTAINING' named entity 'LESION' named entity 'SIMILARITY' named entity 'INSULT' named entity 'DEVELOPS' named entity 'FORMING' named entity 'AXONAL DAMAGE' named entity 'RECENTLY' named entity 'FACT' named entity 'INFECTIONS' named entity 'TRIGGERING' named entity 'DEMYELINATION' named entity 'DAMAGE' named entity 'MULTIPLE SCLEROSIS' named entity 'INSIDE' named entity 'DEMYELINATION' named entity '282' named entity 'HUMAN T-LYMPHOTROPIC VIRUS 1' named entity 'WHITE MATTER' named entity 'SECONDARY' named entity 'TRANSECTION' named entity 'POSSIBILITY' named entity '27S' named entity 'RAISED' named entity 'AXONS' named entity 'SECONDARY DAMAGE' named entity 'HAVE' named entity 'ANIMAL MODEL' named entity 'NORMAL' named entity 'UNEXPECTED' named entity 'END' named entity 'SPREAD' named entity 'HERPES SIMPLEX VIRUS' named entity 'SPINAL CORD' named entity 'PRESENT' named entity 'VIRUS' named entity 'EVENT' named entity 'CAUSE' named entity 'CONTRIBUTE ' named entity 'VIRUS' named entity 'EITHER' named entity 'OLIGODENDROCYTE' named entity 'RESULT' named entity 'CELL' named entity 'PATHOLOGY' named entity 'TRIGGER' named entity 'WHERE' named entity 'SCI' named entity 'RATHER' named entity 'HERE'

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