Blocking a key protein boosts nerve regrowth and functional recovery in mice

Scientists at the Icahn School of Medicine at Mount Sinai discovered that the aryl hydrocarbon receptor (AHR) acts as a brake on the ability of adult neurons to regenerate damaged axons. In experiments where AHR activity was eliminated or inhibited with drugs, injured mice exhibited more robust axon regrowth and restored locomotor and sensory function after both peripheral nerve damage and spinal cord injury. The researchers explained that active AHR favors cellular stress management and protein quality control, which inadvertently limits the production of growth-related proteins.

Suppressing AHR triggers a shift toward protein synthesis and activation of pathways, including HIF-1α, that support regeneration. Because AHR inhibitors are already in clinical trials for other diseases, the findings raise the prospect of repurposing such compounds for nerve-repair therapies, though further studies are needed to determine optimal timing, dosage, and safety in humans.