Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Histo-clinical variation in multiple sclerosis: Heterogeneous proteolytic immunogenic processing.

Fred C Westall1

  • 1Institute for Disease Research, P.O. Box 890193, Temecula, CA 92589-0193, USA. fcwestallidr@adelphia.net

Medical Hypotheses
|October 21, 2005
PubMed
Summary

Multiple sclerosis (MS) variation may stem from how proteases process myelin proteins. This hypothesis explains the unpredictable relapses and varied symptoms seen in MS patients.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

A response to "Association of an EAAT2 polymorphism with higher glutamate concentration in relapsing multiple sclerosis".

Journal of neuroimmunology·2008
Same author

Abnormal hormonal control of gut hydrolytic enzymes causes autoimmune attack on the CNS by production of immune-mimic and adjuvant molecules: A comprehensive explanation for the induction of multiple sclerosis.

Medical hypotheses·2006
Same author

Cell proliferation inhibition in remitting multiple sclerosis CSF.

European neurology·2006
Same author

Molecular mimicry revisited: gut bacteria and multiple sclerosis.

Journal of clinical microbiology·2006
Same author

Integrating theories of the etiology of Crohn's disease on the etiology of Crohn's disease: questioning the hypotheses. William M. Chamberlin, Saleh A. Naser Med Sci Monit, 2006; 12(2): RA27-33.

Medical science monitor : international medical journal of experimental and clinical research·2006
Same author

Molecular mimicry or structural mimicry?

Molecular immunology·2005

Area of Science:

  • Neuroimmunology
  • Proteomics

Background:

  • Multiple sclerosis (MS) exhibits significant histo-clinical variation, including unpredictable relapses and diverse initial symptoms.
  • Current theories, suggesting MS is a collection of diseases, fail to adequately explain this wide spectrum of clinical presentations.
  • MS appears as a continuum of disease courses rather than distinct, well-defined disease types.

Purpose of the Study:

  • To propose a novel hypothesis explaining the histo-clinical variation in multiple sclerosis.
  • To investigate the role of proteolytic processing of myelin components in MS pathogenesis.
  • To offer a framework for understanding the unpredictable nature of MS progression.

Main Methods:

  • The study presents a hypothesis based on the variable proteolytic processing of potential myelin immunogens.

Related Experiment Videos

  • It discusses the role of intracellular and extracellular proteases in the central nervous system (CNS).
  • The hypothesis considers the varying concentrations and locations of proteases within the CNS.

    • Main Results:

    • Variable proteolytic processing of myelin proteins can lead to the presentation of different immunogenic peptides to the immune system.
    • Differences in protease location, concentration, and control can result in the presentation of varying numbers and types of immunogens at different times and locations.
    • This dynamic presentation of immunogens by proteases offers a potential explanation for the variable initial and subsequent symptoms observed in MS.

    Conclusions:

    • Histo-clinical variation in MS is hypothesized to be driven by variable proteolytic processing of myelin-derived immunogens.
    • Protease activity within the CNS dictates the presentation of immunogenic peptides, influencing disease presentation and progression.
    • This hypothesis provides a unified explanation for the diverse clinical spectrum of multiple sclerosis.