A genetic mechanism uncovered by neurology researchers at the University of California, San Francisco, could explain why some patients with multiple sclerosis progress more rapidly to a severe stage of the disease while other patients progress more slowly.
In a mouse model of MS, the researchers found that the absence of the gene Tob1 in CD4+ T cells, a type of immune cell, was the culprit behind early onset of a more serious form of the disease.
MS is an inflammatory disease in which protective myelin sheaths that coat nerve fibers in the brain and spinal cord are damaged and ultimately stripped away--a process known as demyelination. The disease course can vary greatly from person to person, and patients can experience a wide range of cognitive and neurological symptoms.
The researchers genetically engineered mice to be deficient of the Tob1 gene, previously found to be linked to MS when it appears in low amounts. When the researchers induced an MS-like disease in the animals, the genetically engineered mice developed a more aggressive form of the disease much earlier than the normal mice did. Further experiments revealed the likely cause was that the animal's CD4+ T cells were lacking the Tob1 gene. Mice lacking the gene developed earlier and more severe MS than mice with normal Tob1 expression in all cells, including CD4+.
The study was published June 24 in the Journal of Experimental Medicine.
The UCSF team's findings could be the groundwork scientists need to develop a test that predicts the course and severity of MS in different patients, ultimately helping physicians tailor personalized therapies.
- here's the press release
- check out the study abstract