In ALS mice, microglia eat living motor neurons

In the spinal cords of mice with ALS, microglia were not simply cleaning up dead tissue. The Salk Institute team found these resident immune cells engulfing living motor neurons, the cells that carry movement signals from the brain to muscles. The study, published in Nature Communications on August 15, 2026, identifies an unexpected route by which inflammation may worsen the disease.

The route runs through TAM receptors, proteins that normally help the immune system remove dying cells. Greg Lemke, the Salk scientist who discovered the TAM family, describes dying cells as displaying an “eat me” signal. In the SOD1 mouse model—the most widely used mouse model of ALS—the signal appeared on motor neurons that were still alive. Microglia responded, and their levels of the TAM proteins Axl and Mer rose.

The researchers then removed Axl and Mer from the mice. Microglia no longer accumulated as many eaten motor neurons, and the animals retained better muscle control. The result carried a complication: the mice became sicker faster but lived longer. That split outcome is one reason the researchers caution against simply eliminating the TAM system, which also operates elsewhere in the body.

So what changes concretely? The work gives ALS researchers a specific cellular mechanism to test rather than treating microglial activation as a single, unexplained signal. It could help guide therapies that address both TAM activity and the underlying mechanisms of ALS, but the evidence remains limited to mice; it does not establish a treatment for the around 35,000 Americans currently affected by the disease.