Back's lab provided the team with tissue cultures of immature rat oligodendrocytes. The researchers then applied HA to these cells which indeed kept the immature cells from maturing into myelin-producing cells. In another key experiment, Sherman and Back confirmed in another animal model of MS that injection of the HA into damaged myelin prevented myelin from reforming where it had already been destroyed. Conversely, they showed that reducing HA levels or making the HA inactive allows myelin to once again form.
"It is our hope that we can interfere with this disease process at one or multiple stages," explained Back. "Of course for those already battling a myelin-destroying disease, you would want to try and promote the return of myelin-forming cells. This general area of research is of particular interest to me in my attempts to counteract the white matter brain damage that is often associated with premature birth and can lead to a form of cerebral palsy (CP). Our early findings have shown that scar tissue in the brains of premature infants who die during intensive care also produces HA. We believe the HA may also prevent the production of myelin-producing cells and be related to the motor impairment seen in CP. My hope is that this work will benefit a wide range of patients from premature infants to stroke victims to those suffering from debilitating neurological diseases such as MS where repair of damaged myelin does not occur."
Sherman shares this hope. "This discovery has revealed a target for therapies and opens the door to the exciting possibility that we may, one day, be able to not only stop disease progression but also repair damage that is already there. The future efforts of our three labs will be aimed at exactly that goal. "
"The work of these investigators offers new hope to people with MS and their families," said Na