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==Overview==
Overview


==Historical Perspective==
==Historical Perspective==


* Acute disseminated encephalomyelitis has experimental evidence suggests that both primary autoimmune responses and immunological responses triggered by infection may play a role in central nervous system inflammation and demyelination. Clinically and histopathologically, two animal models closely resemble.
* To begin, experimental autoimmune encephalomyelitis (EAE) is commonly utilized to investigate the underlying disease processes, after immunization with CNS homogenate or encephalitogenic myelin peptides emulsified in Freund complete adjuvant. Inflammatory demyelinating lesions can be seen histopathologically in the brains and spinal cords of affected animals.
* Theiler murine encephalomyelitis, which was first utilized as an animal model in the 1930s, has been used to investigate infectious and parainfectious pathways that may play a role in disease etiology.
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==References==
==References==
{{Reflist|2}}
{{Reflist|2}}

Revision as of 21:02, 27 January 2022

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Overview

Historical Perspective

  • Acute disseminated encephalomyelitis has experimental evidence suggests that both primary autoimmune responses and immunological responses triggered by infection may play a role in central nervous system inflammation and demyelination. Clinically and histopathologically, two animal models closely resemble.
  • To begin, experimental autoimmune encephalomyelitis (EAE) is commonly utilized to investigate the underlying disease processes, after immunization with CNS homogenate or encephalitogenic myelin peptides emulsified in Freund complete adjuvant. Inflammatory demyelinating lesions can be seen histopathologically in the brains and spinal cords of affected animals.
  • Theiler murine encephalomyelitis, which was first utilized as an animal model in the 1930s, has been used to investigate infectious and parainfectious pathways that may play a role in disease etiology.



References