Daily Archives: March 17, 2016
Researchers from King’s College London and the University of Oxford have identified a molecular signal, known as ‘neuregulin-1’, which drives and enables the spinal cord’s natural capacity for repair after injury.
The findings, published today in Brain, could one day lead to new treatments which enhance this spontaneous repair mechanism by manipulating the neuregulin-1 signal.
Every year more than 130,000 people suffer traumatic spinal cord injury (usually from a road traffic accident, fall or sporting injury) and related healthcare costs are among the highest of any medical condition – yet there is still no cure or adequate treatment.
Following spinal cord injury, most patients experience an exaggeration of muscle tone called spasticity, which frequently leads to physical disability.
A team at the Institut de Neurosciences de la Timone (CNRS/Aix-Marseille Université) has just identified one of the molecular mechanisms responsible for this phenomenon. It has also proposed two therapeutic solutions that have proved conclusive in animals, one of which will be tested during phase II clinical trials as early as this year. This work, published in Nature Medicineon 14 March 2016, thus opens new therapeutic avenues to reduce this physical disability.
Twelve million people throughout the world suffer from a motor disorder called spasticity.
NEW YORK, March 17, 2016 /PRNewswire-USNewswire/ — United Spinal Association is working with MedStar National Rehabilitation Hospital and Children’s National Medical Center to learn more about the experiences of people who use intermittent catheterization and who experience urinary symptoms frequently.
The research team at MedStar National Rehabilitation Hospital, located in Washington, DC (*participants can be located anywhere in the USA), noticed during a past study that people with bladder dysfunction due to spinal cord injury or disease (SCI/D) had much less Lactobacillus (a ‘healthy’ bacteria) in their urine, compared with those who didn’t have SCI/D.