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    Interleukin-6 (IL-6) drives cancer cachexia by activating brainstem neurons. Blocking IL-6 in the brain prevents cachexia and extends lifespan in mice, revealing a new therapeutic target.

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    Area of Science:

    • Neuroscience
    • Oncology
    • Physiology

    Background:

    • Interleukin-6 (IL-6) is implicated in cancer-associated cachexia.
    • The precise mechanism by which peripheral IL-6 affects the brain in cachexia is unclear.

    Approach:

    • Investigated IL-6's role in cancer cachexia using mouse models.
    • Focused on neurons in the area postrema (AP), a hindbrain circumventricular structure.
    • Utilized IL-6 neutralization, CRISPR/dCas9 interference, and neuronal silencing techniques.

    Key Points:

    • Circulating IL-6 rapidly enters the AP and activates neurons.
    • Tumors increase IL-6, leading to AP neuronal hyperactivity.
    • Neutralizing IL-6 in the brain or targeting IL-6 receptor signaling in AP neurons prevents cachexia and prolongs survival.
    • Silencing Gfral-expressing AP neurons also ameliorates cachectic phenotypes.

    Conclusions:

    • The AP is a critical brain region mediating IL-6's cachexia-inducing effects.
    • Targeting AP neurons offers a potential strategy for treating cancer-associated cachexia.