Jennifer Sabo is investigating how a specific molecule abundant during myelin injury inhibits the natural repair process to exacerbate the neural scarring characteristic of MS.
One of the best opportunities to treat MS is to boost the body’s natural ability to repair itself. There are two ways to do this: the first is to increase and protect the molecules involved in repair, and the second is to stop those molecules, which inhibit the process.
“My aim is to identify regenerative therapeutics for MS. A key outcome of this work will be to understand how we can control these inhibitory molecules called ‘bone morphogeneic proteins’, or BMPs, to stimulate natural remyelination of neurons,” says Jennifer.
BMPs have been shown to decrease oligodendrocyte production. Oligodendrocytes are the myelin producing cells, that remyelinate damaged neurons. However, the role of BMPs in the development of new oligodendrocytes is not well understood. Injury appears to increase the amount of BMPs in the area where neural stem cells reside. This leaves the possibility that BMP ‘antagonists’, molecules that limit the negative effects of BMPs, could prove to be beneficial treatments.
In the first instance, Jennifer will focus on the regulation of BMP signalling during myelin damage and repair. She will examine effects of inhibiting BMP signalling during demyelination to determine whether oligodendrocyte production is increased.
Jennifer Sabo is a scholar gaining her scientific training investigating the role that Bone Morphogenic Proteins (BMPs), secreted molecules in the brain, play in myelin injury and repair. BMPs have been shown to inhibit the production of oligodendrocytes, the myelin-producing cells in the brain and spinal cord, that repair damaged nerves.
Jennifer’s work in particular focuses on inhibiting BMP signalling during myelin injury to increase the production of oligodendrocytes to enhance repair in MS.
In an animal model of MS, Jennifer has shown that BMPs are actively signalling in the stem cell area and in acute demyelinating lesions in the brain. In acute lesions, BMP signalling is significantly increased in the myelin producing cells.
Jennifer has established that BMP activity is increased in oligodendrocyte stem cells in an animal model of MS. She also found that by delivering Noggin, an inhibitor of BMPs, to the brain of diseased mice she could increase oligodendrocyte regeneration and myelin repair.
“I have more work to do to investigate how modulating BMP activity might be combined with other growth factors to further enhance myelin repair in brain lesions,” said Jennifer.
Jennifer’s outstanding progress helped her to gain a competitive Miller Travel Fellowship from Florey Neuroscience Institutes to attend the annual meeting of the American Society for Neurochemistry in March 2011 and to visit three MS research laboratories in the USA.
“It was an incredible opportunity to present my research at a cutting-edge international neuroscience
forum,” said Jennifer. “During my laboratory visits, I had valuable in depth discussions about my research which further enhanced my knowledge and prepared me for a career in MS research.”
Updated: 04 January, 2008