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Updated: Aug 17, 2026

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
08:47

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

Published on: May 8, 2016

Is multiple sclerosis an age-dependent host response to measles?

M Alter

    Lancet (London, England)
    |February 28, 1976
    PubMed

    Insights

    Multiple sclerosis (M.S.) may be an age-dependent immune response to measles infection. Later measles exposure, rather than early childhood, appears to increase M.S. risk.

    Area of Science:

    • Neurology
    • Immunology
    • Epidemiology

    Background:

    • Multiple sclerosis (M.S.) is a neurological disorder with an unclear etiology.
    • Measles infection is known to have age-dependent effects on the immune system and neurological outcomes.
    • Previous studies suggest a link between measles exposure timing and neurological conditions.

    Purpose of the Study:

    • To investigate the hypothesis that multiple sclerosis (M.S.) is an age-dependent host response to measles infection.
    • To explore the relationship between the age of measles acquisition and the risk of developing M.S.

    Main Methods:

    • Review of existing evidence on measles' age-dependent effects in animals and humans.
    • Analysis of studies on immigrant populations and measles exposure.
    • Examination of retrospective data comparing measles history in M.S. patients and controls.

    Main Results:

    • Animal studies show age-dependent responses to measles.
    • Human data indicate age-dependent risks for subacute sclerosing panencephalitis and measles encephalitis.
    • M.S. risk appears associated with measles exposure at or before adolescence, not infancy.
    • Geographical variations in M.S. prevalence correlate with typical age of measles acquisition.
    • Retrospective studies suggest M.S. patients had measles later in life compared to controls.

    Conclusions:

    • The findings support the hypothesis that M.S. may result from an age-dependent host response to measles.
    • Potential mechanisms involve immune system maturation or changes in target cell metabolism.
    • Widespread measles vaccination programs may lead to a future decline in M.S. rates.

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