Glutamate is a common chemical in the
nervous system, which neurons use to send signals to other neurons. But,
like many things, glutamate has to be present in the right amount to work:
Too little leads to a lack of signalling, too much to the death of the nerve
cells that receive the signal.
Evidence from studies of people with MND points to
an overabundance of glutamate in the nervous system. This may result from
inadequate transport of glutamate away from nerve cells after it has
finished its signalling work. Experiments suggest a defect could also lie in
excess production or release of glutamate by the sending cells, or it could
result from defects in glutamate receptors on the receiving cells
MND Causing Genes
Genes that, when flawed, can lead to MND, have
been noted on chromosomes 2, 9, 15, 18 and the X chromosome. More mappings,
identifications and greater understanding of specific genes are expected as
Most X-linked mutations affect males (who only have
one X chromosome, paired with a Y chromosome) but rarely affect females (who
have two X chromosomes, one of which usually doesn't have the mutation).
However, X-linked mutations can sometimes affect females.
A SEARCH FOR TREATMENTS AND A CURE
medications are being tested for potential benefits in MND.
which has been on the market for MND since the mid-1990s, is a glutamate
inhibitor, and other drugs that interfere with the synthesis, release or
cellular reception of glutamate are being studied or tested
THE LATEST ON RESEARCH FROM THE USA MAY 2002
There is strong evidence that the antibiotic,
Inocycline, is proving useful in the treatment of neurodegenerative
diseases. Early indications are that this antibiotic is effective in
the treatment of Huntington's Disease and researchers are confident that it
will prove useful in slowing down the process of ‘programmed cell
death’ which is particularly excessive in MND.
Some researchers are now of the opinion that
Riluzole, the only approved drug used in the treatment of MND, may not be
targeted at the best area of the brains nerve cells to control the toxic
glutamate. Drugs to be developed in the future, they suggest, should target
glutamate control at receptors rather than at point of release. This it is
hoped, will extend life expectancy from a few months, as in the case of
Riluzole, into a few years.