Generating Oligodendrocytes to Spur Remyelination
Researchers here investigate a way to generate more oligodendrocytes in the brain, the cells responsible for creating the myelin sheathing essential to correct function of the nervous system. The presence of more of these cells improves the pace of myelin generation, which may form the basis for therapies to treat the medical conditions that involve accelerated loss of myelin. It is also the case that some loss of myelin maintenance will occur for all of us in old age due to growing cellular dysfunction and damage. This likely contributes to cognitive decline and other manifestations of old age, so it is worth keeping any eye on the development of potential treatments in this area.
Scientists found that deleting from the adult brain a protein necessary for early development actually fosters the growth of cells that generate myelin, the important protective coating neurons need to function. The research on lab animals provides new insight into how critical brain cells are generated. The finding may lead to improved treatments for brain injury, demyelinating diseases, certain developmental diseases and brain tumors. Researchers studied Nuclear Factor I X (NFIX), a transcription factor - a protein that turns genes on and off. NFIX is required for normal development of the early brain and it's known that losing NFIX before birth results in a number of rare human diseases, characterized by severe developmental and physiological defects. However, the new study shows that the loss of NFIX is necessary at a certain point in order for some brain cells to develop normally.Oligodendrocytes surround neurons, which transmit electrical signals in the brain, protecting them from damage and speeding the transmission of those signals. The research shows that as neural stem cells differentiate into oligodendrocytes, the expression of NFIX decreases, apparently an essential step in the normal formation of the myelin-making cells. "In terms of a treatment, this could lead to the development of a small molecule that could be used to shut off NFIX activity in MS patients, thus promoting the growth of more oligodendrocytes." This study and previous ones have found that loss of NFIX could also increase the growth of adult neural stem cells, which, in turn, generate new neurons in adult animals. "This could also help us find ways to stimulate new neuron production in diseases where neurons die, such as in Alzheimer's and Parkinson's diseases and in spinal cord injury." The researchers' next step is to learn which genes are regulated by NFIX, and the best way to promote this increase in both oligodendrocytes and neural stem cells.