Blocking IL-6 from Binding to Brain Neurons Shows Promise for Cancer Cachexia Treatment

Cold Spring Harbor Laboratory (CSHL) researchers have uncovered a potential treatment for cancer cachexia, a lethal wasting disease affecting 50% to 80% of cancer patients. The research, led by Professor Bo Li and published in Nature Communications, focuses on the role of Interleukin-6 (IL-6) in causing severe brain dysfunction and cachexia in cancer patients.

In healthy patients, IL-6 plays a crucial role in natural immune response. The molecules circulate throughout the body. When they encounter a possible threat, they alert the brain to coordinate a response. Cancer disrupts this process. Too much IL-6 gets produced, and it begins binding to AP neurons in the brain. “That leads to several consequences,” Li says. “One is animals and humans alike will stop eating. Another is to engage this response that leads to the wasting syndrome.”

The CSHL team's innovative approach involved blocking IL-6 from binding to AP neurons in mice. They employed two strategies: neutralizing IL-6 with custom antibodies and using CRISPR to reduce IL-6 receptors in AP neurons. Both methods yielded promising results, with mice resuming eating, halting weight loss, and experiencing increased longevity.

Professor Li expressed amazement at the brain's power in regulating bodily systems: “The brain is so powerful in regulating the peripheral system. Simply changing a small number of neurons in the brain has a profound effect on whole-body physiology."

This discovery opens new avenues for treating cancer cachexia in humans. The research team, collaborating with other CSHL professors, is now focused on translating these findings to human patients. Li emphasizes the potential impact: "If we can use what we've learned to prevent or treat cachexia, we can dramatically increase patients' quality of life."