Whom is going to update the stroke strategy to add this to the 'figure this out' category and put it in someones' responsibility column? With no responsibility nothing ever gets solved in stroke. This is simple management 101, when are our stroke associations going to join the useful world and accomplish a needed stroke rehabilitation task?
http://www.alphagalileo.org/ViewItem.aspx?ItemId=150453&CultureCode=en
Inflammatory processes occur in the brain in conjunction with stroke
and neurological diseases such as Alzheimer’s and Parkinson’s disease.
Researchers from Lund University and Karolinska Institutet in Sweden, in
close cooperation with a group led by Professor José L. Venero at the
University of Seville, have presented new findings about some of the
‘key players’ in inflammation. In the long term, these findings could
lead to new treatments.
One of these key players is a receptor called TLR4. The receptor
plays such an important role in the body’s innate immune system that the
researchers who discovered it were awarded the 2011 Nobel Prize in
Physiology or Medicine. The other key player is a protein called
galectin-3, which is absent in healthy brains but present in a brain
suffering ongoing inflammation.
“We have demonstrated that galectin-3 is secreted by microglial
cells, a type of immune cell in the brain. The protein binds to the TLR4
receptor and amplifies the reactions that lead to inflammation. More
galectin-3 is produced and binds to the immune cells, and the immune
response is further intensified in a self-sustaining process”, explained
Tomas Deierborg, associate professor at Lund University.
The researchers have demonstrated the importance of the link between
the two ‘key players’ using various different methods and in laboratory
tests, animal experiments and human trials. They have shown that mice
genetically modified to be incapable of synthesising galectin-3 show a
lower inflammatory response and less brain damage after a heart attack.
Mice with a model of Parkinson’s disease also suffer less brain damage
if they do not have the gene for galectin-3.
The researchers have also observed the interaction between galectin-3 and TLR4 in the brains of people who died of a stroke.
“We believe that this link could be part of the explanation for the
residual disability that stroke patients often experience. High levels
of galectin-3 remain in the brains of these patients long after the
stroke, which may explain why the inflammatory response continues to
cause damage and does not subside”, said Miguel Angel Burguillos,
currently working at Queen Mary University of London.
Galectin-3 is already a target for pharmaceutical companies trying to
develop agents that hinder the harmful effects of the protein in
neuroinflammatory diseases. The new findings on the effects and role of
the protein in a diseased or damaged brain should provide important
input to this work.
“Previously, it was acknowledged that galectin-3 contributed to the
inflammatory response but the mechanism wasn’t clear. The protein is not
present in a healthy brain, only in one that is suffering an
inflammatory response. Now that we understand the mechanism, this will
make it easier to develop more effective treatments”, said Dr Deierborg.
About the study:
Dr Burguillos is currently working at Queen Mary
University of London, but carried out the work on galectin-3 and TLR4
during his time as a postdoctoral fellow at Lund University and
Karolinska Institutet. The research in Lund has been led by Tomas
Deierborg and at KI by Bertrand Joseph. The University of Seville also
participated in the research, led by José L. Venero. The results have
recently been published in the journal Cell Reports.
http://www.cell.com/cell-reports/abstract/S2211-1247%2815%2900140-0
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