We have nothing like this for stroke because we have NO leadership pushing any BHAGs(Big Hairy Audacious Goals)
And the boards of directors must be ok with such incompetence.
Meanwhile stroke survivors don't get any better therapy or closer to recovery.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=165441&CultureCode=en
A study publish in the journal CELL indicates that two genes
associated with Parkinson's disease (PD) are key regulators of the
immune system, providing direct evidence linking Parkinson's to
autoimmune disease.
A team of scientists led by Dr. Michel Desjardins from the University
of Montreal and Dr. Heidi McBride from the Montreal Neurological
Institute and Hospital (MNI) at McGill University have discovered that
two genes associated with Parkinson's disease (PD) are key regulators of
the immune system, providing direct evidence linking Parkinson's to
autoimmune disease.
Using both cellular and mouse models, the team has shown that
proteins produced by the two genes, known as PINK1 and Parkin, are
required to prevent cells from being detected and attacked by the immune
system.
When PINK1 and Parkin are dysfunctional, as is the case in a subset
of Parkinson’s patients, cells display small parts of proteins at their
surface, known as antigens, derived from mitochondria. The presence of
these antigens at the cell surface causes the activation of immune cells
called lymphocyte T cells. These T cells, which can enter the brain,
have the ability to destroy any cell displaying the mitochondrial
antigens on their surface.
Parkinson’s is caused by the death
of dopamine-producing neurons in the brain. An overactive immune system
due to dysfunctional PINK1 and Parkin genes could explain why
dopaminergic neurons die in Parkinson’s patients. This indicates that
Parkinson’s may be one of many autoimmune diseases, including multiple
sclerosis, Type 1 diabetes, rheumatoid arthritis, and lupus. An
autoimmune disease is one in which the body’s own immune system attacks
healthy cells.
Researchers suspected that mitochondria, organelles within cells that
are responsible for the production of energy and other metabolites,
play a role in Parkinson’s. It was widely believed that mitochondria
become damaged in Parkinson’s patients, creating a toxic build-up of
broken mitochondria that eventually leads to neuron cell death. However,
it has been difficult to provide evidence that this is effectively
happening in animal models.
The new findings of the Desjardins/McBride teams linking PD to
autoimmune mechanisms, published in the prestigious journal Cell on June
23, have been validated in a mouse model of Parkinson's disease where
PINK1 or Parkin are absent.
“Clinicians have shown that the immune system is activated in the
brain of PD patients,” says Dr. Diana Matheoud, a postdoctoral fellow
from the University of Montreal and the article’s first author. “Our
study explains how an attack by the immune system may be responsible for
the destruction of dopaminergic neurons during the disease. We are
currently testing whether autoimmune mechanisms lead to the loss of
dopaminergic neurons in mice, and developing systems to extend our study
to human neurons."
“Antigen presentation was not believed to play a direct role in
Parkinson's disease,” says McBride. “While most laboratories are
following the trail of the ‘toxic mitochondria’ model, our path led us
to observe Parkinson's disease from a different point of view. Our
approach, centered on the immune system, led us down a different road
where we were able to observe that autoimmunity is likely to play an
important role in the progression of the disease.”
Now that a link has been established between two key genes involved
in the pathology of Parkinson’s disease and autoimmune mechanisms, the
next step is to develop drugs that can limit the presentation of
mitochondrial antigens. Remarkably, the mechanism by which mitochondrial
antigens are presented involves a process of vesicle formation,
originally described by the McBride group, offering molecular targets
for the development of new drugs in an effort to block this process.
The researchers’ findings may also lead to better treatments for
other diseases. “We think that our study is paradigm shifting because we
have identified a new biological pathway linking mitochondria to immune
mechanisms in Parkinson’s disease. This opens the possibility to use
therapies based on modulation of the immune system, something already
done for the treatment of other diseases,” says Desjardins.
“Interestingly, the role played by PINK1 and Parkin in limiting the
presentation of mitochondrial antigens may not only regulate a process
that impact Parkinson’s disease, but may also affect other autoimmune
diseases like diabetes and lupus, and primary biliary cirrhosis, where a
link to mitochondrial antigen presentation has been observed.”
“This paper suggests an entirely novel mechanism by which these
recessive, inherited mutations may lead to neurodegeneration,” says Jon
Stoessl, Professor and Head of Neurology at the University of British
Columbia & Vancouver Coastal Health, and former Director of the
Pacific Parkinson’s Research Centre. “There has been much interest in
the potential role of inflammation in PD. Previous studies on Parkin and
PINK1 have focused on disruption of mitochondrial housekeeping
functions. While the current findings may clearly be related, they
suggest an entirely novel approach to the development of targeted
therapies. It should be remembered that these are rare causes of
Parkinson's disease and the relevance to dominantly inherited and
sporadic forms of disease remains to be determined.”
This research was funded with the help of the Canadian Institute for
Health Research and the Canadian Research Chairs program of Canada.
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