Re: How Brain Stem Cells Develop Into Cells Which Repair Damaged Tissue
- From: Sylvia <Sylv772003@xxxxxxxxx>
- Date: Fri, 10 Jul 2009 13:51:59 -0700 (PDT)
Tick;
Exciting Indeed...
Insight Into How Brain Stem Cells Develop Into Cells Which Repair
Damaged Tissue
03 Jul 2009
This is exciting! Thanks for posting this!
Sylvia
The joint research, funded by the National Multiple Sclerosis Society
and the UK MS Society as well as the National Institutes of Health and
Howard Hughes Medical Institute, was conducted by scientists at the
University of California San Francisco (UCSF) and University of
Cambridge and was published in the journal Genes and Development.
Multiple sclerosis is an autoimmune disease which is caused by the
body's immune system attacking nerve fibres and their protective
insulation, the myelin sheath, in the central nervous system. This
damage prevents the nerves from 'firing' properly, and then leads to
their destruction, resulting in physical and intellectual
disabilities.
It is currently thought that two components determine clinical
outcomes in MS. First, it is important to stop ongoing damage (mainly
achieved by controlling inflammation in the central nervous system).
The second is to repair the damage that has occurred to the protective
myelin sheaths surrounding the nerve fibres (this involves a
regenerative process called remyelination in which new myelin sheaths
are restored to nerve fibres).
While there exist several effective treatments to reduce inflammatory
damage, no treatments are available to augment remyelination to repair
the damage to nerve fibres. Critical to the development of such repair
therapies is to understand how the brain's own stem cells can replace
the myelin forming cells (oligodendrocytes) lost in the disease.
During early stages of the disease the brains own stem cells are
surprisingly good at repairing damage in MS. However, for reasons that
until now have not been well explained, they become less efficient as
the disease progresses.
In this study the researchers have identified the Wnt pathway, which
plays an active role in the maintenance and proliferation of stem
cells, as a crucial determinant of whether oligodendrocytes can
efficiently make myelin. Their studies demonstrate that if the Wnt
pathway is abnormally active, then the process is inhibited. This
opens up the exciting possibility that the repair can be enhanced in
MS patients by drugs that block the Wnt pathway.
Professor Robin Franklin from the University of Cambridge, a co-senior
author of the study, explained the significance of their findings:
"The pathway we identified plays a critical role in whether repair to
the damaged cells will or will not occur. Interestingly, mutations in
this particular pathway are also involved in several cancers. In this
regard, drugs that inhibit this pathway from signaling have been
sought which might suppress tumour growth. These same drugs may also
find a role in promoting repair in MS."
Lead author of the study, Stephen Fancy, PhD, a postdoctoral fellow in
the lab of co-senior author David Rowitch, MD, PhD, a Howard Hughes
Medical Institute Investigator at the University of California, San
Francisco, said: "We believe we have made a significant step forward
in understanding why repair might fail in neurological diseases such
as MS by identifying a pathway which inhibits the myelin repair
process," said the
MS Society Director of Research, Jayne Spink, said: "We are delighted
with the outcome of this outstanding research, which gives us greater
knowledge of the mechanics of MS. This works opens up new avenues of
research and lends itself to more study. Being able to uncover the
secrets behind the damage caused in MS will take us forward in our
understanding of this debilitating condition."
"Our studies work have implications for other diseases," said UCSF's
Rowitch. "In a condition called periventricular leukomalacia (PVL),
which can lead to cerebral palsy in extremely premature infants,
recent studies show a similar inability of oligodendrocytes to perform
their important repair function. In respect to failed myelin repair,
we see a parallel between the chronic demyelinated plaques of multiple
sclerosis and the lesions of PVL."
Source:
Genevieve Maul
University of Cambridge
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Article URL:http://www.medicalnewstoday.com/articles/156231.php
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