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Updated: Feb 10, 2026

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
Published on: July 19, 2019
Multiple sclerosis and prions
1Department of Internal Medicine, Henry Ford Hospital, Detroit, MI 48202.
Abstract:
The etiology of Multiple Sclerosis (MS) is unknown. Existing epidemiologic data suggests that MS can be an infectious disease. MS used to be classified as one of the 'slow infections'--many of these are caused by prions. Prions are small, proteinaceous, infectious particles--distinguished from viruses by the absence of intrinsic nucleic acids. In a contrast to the 'classic' prional diseases (Kuru, Scrapie or Creutzfeldt-Jacob Disease) that in CNS affect primarily neurons, the 'target' cell in MS is an oligodendrocyte. This may explain differences in disease presentation. This paper presents a pathophysiological model of MS based on the assumption that MS is a prional disease. Processes leading to the demyelination in Multiple Sclerosis seem also to involve lymphocytes, astrocytes and macrophages as well as the interferon system.
Insights
Multiple Sclerosis (MS) may be a prion disease, a type of slow infection. This theory explains MS pathology, focusing on oligodendrocytes and demyelination, differing from classic prion diseases.
Area of Science:
- Neuroimmunology
- Infectious Diseases
- Neuropathology
Background:
- The exact cause of Multiple Sclerosis (MS) remains unknown.
- Epidemiological data suggests an infectious etiology for MS.
- MS was previously categorized with 'slow infections,' many caused by prions.
Purpose of the Study:
- To present a pathophysiological model of MS.
- To propose that MS is a prion disease.
- To explain the unique cellular targets and disease presentation in MS compared to classic prionopathies.
Main Methods:
- Review of existing epidemiologic data on MS.
- Comparison of prion characteristics with MS pathology.
- Development of a theoretical pathophysiological model for MS.
Main Results:
- Prions, infectious protein particles lacking nucleic acids, are implicated.
- Unlike classic prion diseases affecting neurons, MS targets oligodendrocytes.
- This cellular difference may account for distinct clinical presentations.
Conclusions:
- The proposed model posits MS as a prion disease.
- Demyelination in MS involves oligodendrocytes, lymphocytes, astrocytes, and macrophages.
- The interferon system also appears to play a role in MS pathogenesis.
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