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.

Sunday, October 9, 2011

New research reveals brain's protection mechanism during stroke

My neurons were obviously not very resistant to stroke damage, they keeled over immediately.
http://medicalxpress.com/news/2011-08-reveals-brain-mechanism.html

Neuroscientists have identified a natural protection mechanism in some of the brain's nerve cells during the onset of stroke. The findings, published today in the Journal of Neuroscience, could be used to develop treatments to protect other nerve cell types responsible for speech and movement.

Stroke — the third largest cause of death in the UK — causes disruption to the blood supply to the , depriving nerve cells of oxygen and nutrients. This leads to the death of nerve cells and the consequent loss of the brain's cognitive functions such as speech and movement. However, not all nerve cells are equally susceptible to stroke-induced damage.

The research, led by Dr Jack Mellor from the University of Bristol, examined two types of nerve cell in a part of the brain called the hippocampus — the region linked to memory and navigation. One of these cell types, the CA1 cell, is highly susceptible to damage after stroke whereas the other, the CA3 cell, is much more resistant despite many other similarities between the two cell types.

Dr Mellor, Senior Lecturer in the University's School of Physiology and Pharmacology, said: "We hope that if we can understand why some nerve cells are resistant to stroke damage we may be able to develop strategies to protect those cells that are sensitive."

The researchers found that the CA3 cells possess a mechanism for reducing their susceptibility during, and immediately after, a laboratory-based model for stroke. This mechanism involved making the CA3 cells less sensitive to the neurotransmitter glutamate, which is released in large quantities during stroke, by removing glutamate receptor proteins from the surface of these cells.

The removal of glutamate receptors was triggered by adenosine A3 receptors that are activated by very high levels of the neurotransmitter adenosine found only during stroke conditions. Interestingly, CA1 cells that are susceptible to stroke damage did not have adenosine A3 receptors and did not respond to the stroke model by removing surface glutamate receptors. The findings reveal that CA3 cells possess a mechanism for neuronal protection during stroke.

Dr Mellor added: "Historically, stroke has been very difficult to treat because of its unpredictability and the need to administer drugs within minutes of the onset of a . These problems will not be overcome by our research but our findings do reveal a natural protection mechanism in some , which may be useful in developing treatments to protect other nerve ."

More information: The research, entitled 'Oxygen/glucose Deprivation Induces a Reduction in Synaptic AMPA Receptors on Hippocampal CA3 Neurons Mediated by mGluR1 and adenosine A3 Receptors', is published in the Journal of Neuroscience.

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