According to the Christopher & Dana Reeve Foundation, about two percent of Americans – more than six million people – have some form of paralysis resulting from spinal cord injury.
It is due primarily to the interruption of connections between the brain and spinal cord. Such paralysis and loss of function has long been considered untreatable, but a new approach has, for the first time, induced robust regeneration of nerve connections that control voluntary movement, showing the potential for new therapeutic approaches to paralysis and other motor function impairments and offering hope to sufferers.
In a study on rodents, researchers at UC Irvine (UCI), UC San Diego (UCSD) and Harvard University, achieved this breakthrough by turning back the developmental clock in a molecular pathway critical for the growth of corticospinal tract nerve connections. The corticospinal tract is a collection of axons – the long, slender projections of a nerve cell that conduct electrical impulses – that travel between the cerebral cortex and the spinal cord that is concerned specifically with discrete voluntary skilled movements.
They did this by 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.
Trying to find a way to restore early-developmental-stage cell growth in injured tissue, Zhigang He, a senior neurology researcher at Children’s Hospital Boston and Harvard Medical School, first showed in a 2008 study that blocking PTEN in mice enabled the regeneration of connections from the eye to the brain after optic nerve damage.