Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, March 13, 2012

Genetic study shows that inflammatory protein plays a role in heart disease

We need our researchers to tell us if this would also affect strokes.
http://www.eurekalert.org/pub_releases/2012-03/uoc-gss031212.php

Study suggests that anti-inflammatory drugs could be used to treat cardiovascular disease

A protein involved in inflammation, the interleukin-6 receptor (IL6R), is a contributing cause in the development of heart disease, new research led by the University of Cambridge has discovered. The research was published today, 15 March, in the journal The Lancet.

The findings suggest that targeting the IL6R signalling pathway might therefore be an effective way of combatting heart disease.

Dr Adam Butterworth, who co-led the study from the University of Cambridge, said: "Typically, it can take many years to make safe and effective drugs to target new disease pathways. However, in this case, drugs have been previously developed due to this pathway's involvement in autoimmune disease. In fact, one such drug, Tocilizumab, is already used for treating arthritis, and might therefore be a viable drug for preventing heart disease."

The research, undertaken as part of the IL6R Genetics Consortium and Emerging Risk Factors Collaboration and funded by the British Heart Foundation and the Medical Research Council, analysed human genetic and biomarker data from more than 200,000 participants compiled from 82 previous studies. The research focused on the genetic variant Asp358Ala which is known to affect IL6R signalling pathways involved in the inflammatory response.

The researchers discovered that people who carry the 'Ala' form of the variant have a reduced risk of coronary heart disease (3.4% for each additional copy of Ala that is inherited). Although this genetic change in risk is small, the potential reduction in an individual's risk of heart disease provided by a drug could be much greater.

Dr Butterworth added: "Individuals carrying 358Ala had lower levels of markers of systemic inflammation, suggesting that this variant dampens the inflammatory response. As carriers of this variant also had a decreased risk of heart disease, this strongly indicates that IL6R pathways play a causal role in coronary heart disease."

Nearly 200,000 people die from cardiovascular disease in the UK every year, comprising one in three of all deaths. (Source: British Heart Foundation website).


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