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Related Concept Videos

Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
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Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
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In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...
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Autoimmune Disorders

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Multiple sclerosis - a response-to-damage model.

Bert A 't Hart1, Rogier Q Hintzen, Jon D Laman

  • 1Department of Immunobiology, Biomedical Primate Research Center, Lange Kleiweg 139, 2288 GJ Rijswijk, The Netherlands. hart@bprc.nl

Trends in Molecular Medicine
|May 20, 2009
PubMed
Summary
This summary is machine-generated.

Virus infection may trigger autoimmune neuroinflammation in multiple sclerosis (MS). Lifelong herpesvirus infections create memory T cells that can cause MS years after initial infection, offering new diagnostic and therapeutic targets.

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Area of Science:

  • Neuroimmunology
  • Virology
  • Autoimmune Diseases

Background:

  • The concept of viral triggers for multiple sclerosis (MS)-associated neuroinflammation is widely supported but lacks direct evidence.
  • A proposed mechanism involves asymptomatic herpesvirus infections, such as cytomegalovirus, leading to autoreactive T cells.
  • These T cells may be reactivated by central nervous system (CNS) injury, initiating autoimmune neurological disease.

Purpose of the Study:

  • To investigate the role of antiviral memory T cells in the pathogenesis of multiple sclerosis.
  • To explore the potential of targeting anti-herpesvirus T-cell responses for MS diagnosis and therapy.

Main Methods:

  • Utilizing non-human primate models of multiple sclerosis.
  • Analyzing the T-cell repertoire generated by lifelong asymptomatic herpesvirus infections.

Main Results:

  • Evidence suggests that persistent, asymptomatic herpesvirus infections can generate memory T cells with autoreactive potential.
  • These T cells can be reactivated by CNS injury-related antigens, years post-infection, leading to autoimmune neurological disease.

Conclusions:

  • The study supports a "response-to-damage" model where antiviral memory cells contribute to MS pathogenesis.
  • Elucidating the anti-herpesvirus T-cell repertoire may reveal novel targets for the prevention, diagnosis, and treatment of multiple sclerosis.