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Department of Cellular and Molecular Neuroscience
Department of Neuropathology
Multiple Sclerosis Society of Great Britain and Northern Ireland
E-mail: ukmstissuebank@imperial.ac.uk
Issue Two
(The Bank Statement is also available as a PDF document.)
4. Damage to nerve cells:
Areas that have more nerve cell bodies than myelin appear grey (grey matter) and regions that are richer in myelin look white (white matter). Since some of the symptoms associated with MS, especially disturbances in the so-called “higher” functions (such as memory and concentration) may be caused by damage to nerve cell bodies, the group in Oxford have been looking to see how grey matter is affected in MS. One study looked closely at one grey matter area - the thalamus (the brain’s “telephone exchange”) in tissue donated by eight MS patients and two patients that did not have MS (control subjects).
These are images of the thalamus from a control (left) and an MS donor (right) seen under a microscope. Fewer nerve cell bodies (arrows) are present in the MS sample; there was an overall 35% reduction in the thalamus from the eight MS patients.
Since the loss of nerve cells in the grey matter may contribute to some of the symptoms experienced by individuals living with MS, new therapies need to not only tackle demyelination but also ensure that nerve cell bodies are protected from harm
How is grey matter affected in MS?
Professor Margaret Esiri, University of Oxford, Radcliffe Infirmary
The varied symptoms experienced by people living with MS arise because of the development of discrete areas of damage (lesions) within the CNS. The CNS can be divided into two areas according to the relative proportions of myelin (wrapped around axons) and nerve cell bodies (an axon is a single outgrowth from a nerve cell body along which nerve impulses travel).
5. Myelin damage:
Antibodies in oligoclonal bands might attack myelin
Dr Sandra Amor, BPRC, Rijswijk, The Netherlands
An important test used in the diagnosis of multiple sclerosis is the detection of oligoclonal bands in the cerebrospinal fluid (CSF) that is sampled from a lumbar puncture. The bands are there because antibodies (molecular anchors that are very choosy in what they attach to) are being manufactured in the brain. These are washed away by the fluid that bathes the brain - the CSF. Ever since these bands were discovered, scientists have been striving to identify the compound to which the antibodies are trying to attach. Could the compound be myelin? If yes, then these antibodies could be playing a role in damaging the myelin within MS lesions. Myelin is a complex material made up of many different proteins, fatty molecules and sugars; and so the question is really - are antibodies in oligoclonal bands binding to any “bit” of myelin? The first task for Dr Amor is to prepare myelin from brain tissue and then separate out one particular component – MOG (myelin oligodendrocyte glycoprotein). There are a number of reasons why MOG holds a particular interest for Dr Amor. If a laboratory animal is made to manufacture antibodies to MOG as part of an immune response, then these antibodies attack myelin in the CNS resulting in a disease that is similar to MS. Also, MOG is present on the surface of myelin sheaths where it would be easily reached by antibodies. The only problem is that MOG is present in very small quantities. So currently, Dr Amor is purifying MOG from brain tissue donated by MS patients and from people that did not have MS. Why is it important to identify the exact component of myelin to which the antibodies are binding? Because there are now ways available of switching off the immune system from making antibodies; but remember that antibodies play a vital role in protecting our bodies against invading micro-organisms, so, the trick is only to switch off making those antibodies that may be attacking the myelin.
6. Repair:
Why does remyelination fail?
Professor Catherine Lubetzki, Hôpital de la Salpêtrière, Paris
Although remyelination is a process that occurs naturally within the CNS of people living with MS; this repair process eventually cannot keep up with the demyelination. In order to understand this group’s approach to answering the question “Why does remyelination fail?” we first have to know that when axons are developing during childhood, they stop myelin formation occurring until the time is right by coating themselves in a layer of a “non-stick” molecule called PSA- NCAM (polysialylated-neural cell adhesion molecule). Myelin sheaths can only wrap themselves around the naked axons once they have stopped expressing PSA-NCAM. Could the failure of remyelination in MS lesions be due to the demyelinated axons coating themselves with PSA-NCAM? To answer this, the group looked at the presence of PSA-NCAM on myelinated, demyelinated and remyelinated axons in tissue samples from 24 MS donors and 5 donors that had not had MS (the control subjects). They found that the myelinated axons in normal tissue from MS and control donors did not have PSA-NCAM; nor did the axons in completely remyelinated lesions. However, axons in completely demyelinated lesions were coated with PSA-NCAM. These observations have led the group to suggest that in demyelinated MS lesions, the presence of PSA-NCAM on axons prevents them from being remyelinated. They are now trying to find ways of stopping this molecule from being produced, since this could help the process of myelin repair.
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Division of Neuroscience and Mental Health
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E-mail: ukmstissuebank@imperial.ac.uk