Scientists push forward understanding of multiple sclerosis
New findings by a research team from the University of Edinburgh may help explain why diseases like multiple sclerosis (MS) which attack the myelin sheath – an insulator which protects the body's nervous system - cause such severe symptoms in MS patients. Their discoveries may lead to new ways to help treat patients with MS, it is reported in the journal Neuron today (Thursday, 8 December).
The scientists have made an important breakthrough in understanding how animals with complex nervous systems, such as humans, achieve rapid signalling between their nerve cells. Communication between nerve cells and other organs such as muscles needs to be extremely fast, so that the body responds quickly to instructions from the brain. Electrical signals can travel rapidly from the brain because they 'jump' down nerves using specialised hotspots called nodes.
Professor Peter Brophy of the Centre for Neuroscience Research at the Unversity and leader of the study explained: "It has been known for some time that the location of the nodes along nerves is determined by specialised cells called glia, which surround nerves with a myelin sheath. The nerves of babies are surrounded by these glial cells in the first few years after birth, which ensures proper development of the human nervous system. If nerves do not get their myelin sheath, or if they lose it later because of diseases like MS, the nodes either don't form, or are disrupted, leading to a serious loss of nervous system function, which in turn can lead to blindness, paralysis or even death."
Professor Brophy's team has discovered the key molecules- two proteins found in the gene Neurofascin- that link glial ensheathment of the nerve fibres to the formation of nodes. "We hope that the discovery of these proteins will help us to find ways to improve nerve conduction in patients with conditions where the myelin sheath is attacked," he said.
Source: Eurekalert & othersLast reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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