In PLOS Biology, an Imperial College London-led team presents findings from mouse model experiments linking enhanced CBP/p300 co-activator protein family activation to features consistent with spinal cord regeneration after injury. Following from past results, the researchers followed mouse spinal cord injury models treated with the CBP/p300-activating small molecule TTK21, which acts as an epigenetic regulator. In the months after the severe injury, they found that weekly systemic TTK21 treatment led to an uptick in synaptic plasticity and regenerative signaling in the injury model, along with increased sensory axon growth in the spinal cord and reduced motor axon retraction above the injury site. "The CBP/p300 activator TTK21 … promotes the expression of regenerative signals including some well-established RAGs," the authors note. "This is a potentially exciting discovery since it provides a demonstration that a clinically suitable molecular intervention can promote plasticity and growth in both an acute, as previously shown, and chronic SCI with severe disability, likely by reawakening a dormant regenerative gene expression program."