Tampa, Fla. (Dec, 19 2011) A team of researchers grafting human spinal stem cells into rats modeled with amyotrophic lateral sclerosis (ALS), also known as "Lou Gehrig's Disease," a degenerative, lethal, neuromuscular disease, have tested four different immunosuppressive protocols aimed at determining which regimen improved long-term therapeutic effects. Their study demonstrated that a combined, systematically delivered immunosuppression regimen of two drugs significantly improved the survival of the human spinal stem cells. Their results are published in the current issue of Cell Transplantation (20:8), now freely available on-line at http://www.ingentaconnect.com/content/cog/ct/.
"There are no therapeutic strategies that successfully modify ALS progression or outcome," said study corresponding author Dr. Michael P. Hefferan of the University of California-San Diego Neurodegeneration Laboratory. "Cell-based transplantation therapies have emerged as potential treatments for several neurological disorders, including ALS. However, cell graft survival seems to greatly depend on an accompanying immunosuppression regimen, yet there are differential responses to identical immunosuppressive therapies."
While the reason for this differential response is unclear, the study authors suggest that several mechanisms, including distinct types of acute and inflammatory responses, may be to blame.
Their study aimed at optimizing an immunosuppressive protocol for transplanting human spinal cord cells into presymptomatic ALS G93A rats with the G93A superoxide dismutase (SOD1) mutation. Two drugs, tacrolimus (FK506) and mycophenolate, were used alone and in combination.
"Although FK506 has been used successfully as monotherapy in our previous studies of spinal ischemia, it failed in the present study on ALS," explained Dr. Hefferan, who speculated that inflammation played a role in the fail
'/>"/>
| Contact: David Eve celltransplantation@gmail.com Cell Transplantation Center of Excellence for Aging and Brain Repair Source:Eurekalert |