An estimated 2% of Americans have some form of paralysis resulting from spinal cord injury, and the condition is largely considered permanent as a result of the failure of injured nerve cells to regenerate in the central nervous system. A team from University of California/Irvine (UCI; California, USD), University of California/San Diego (UCSD; California, USA), and Harvard University (Massachusetts, USA) has induced robust regeneration of nerve connections that control voluntary movement after spinal cord injury, showing the potential for new therapeutic approaches to paralysis and other motor function impairments.  The team deleting an enzyme called PTEN (a phosphatase and tensin homolog), which controls a molecular pathway called mTOR that is a key regulator of cell growth. PTEN activity is low early during development, allowing cell proliferation. PTEN then turns on when growth is completed, inhibiting mTOR and precluding any ability to regenerate. As a result, the researchers effectively turned back the developmental clock in a molecular pathway critical for the growth of corticospinal tract nerve connections.   Writing that: “These regenerating [corticospinal tract] axons possessed the ability to reform synapses in spinal segments distal to the injury,” the researchers conclude that: “Modulating neuronal intrinsic PTEN/mTOR activity represents a potential therapeutic strategy for promoting axon regeneration and functional repair after adult spinal cord injury."