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.

Friday, August 2, 2013

Brain Derived Neurotrophic Factor Key Element in Recovery from Stroke

Do you really think anyone is going to push this to a research trial unless we are in charge?
http://www.biotechdaily.com/genomics_proteomics/articles/294744078/brain_derived_neurotrophic_factor_key_element_in_recovery_from_stroke.html
Candesartan, a drug used to reduce blood pressure, has been found to stimulate formation of new blood vessels (angiogenesis) in the brain following stroke, and a recent study has linked this action to increased expression of brain derived neurotrophic factor (BDNF).

BDNF is a member of the neurotrophin family that has been reported to have angiogenic effects and play an important role in recovery after stroke, while candesartan is an angiotensin II type 1 receptor blocker (ARB) that has been to shown to limit ischemic stroke and improve stroke outcome. In experimental stroke, candesartan induced a proangiogenic effect that was partly due to vascular endothelial growth factor (VEGF).

In a recently published study, investigators at the University of Georgia (Athens, USA) described the role of BDNF in the proangiogenic effect of candesartan in the brain under hypertensive conditions.

The investigators treated spontaneously hypertensive rats with candesartan, and brain tissues were collected for quantification of BDNF expression. In addition, human cerebromicrovascular endothelial cells were treated with either low or high doses of angiotensin II alone or in combination with candesartan to assess the effect of candesartan treatment and BDNF involvement in the behavior of endothelial cells.

Results published in the December 4, 2012, online edition of the Journal of Pharmacology and Experimental Therapeutics revealed that candesartan significantly increased the expression of BDNF. In addition, candesartan reversed the antiangiogenic effect of AngII. The observed effects of candesartan were eliminated by neutralizing the effects of BDNF or by blocking the AT2 receptor.

Thus, candesartan blockage of the angiotensin II type 1 receptor, which lowered blood pressure, stimulated the AT2 receptor and increased the secretion of BDNF, which encouraged brain repair through the growth of new blood vessels.

"BDNF is a key player in learning and memory," said senior author Dr. Susan Fagan, professor of pharmacy at the University of Georgia. "A reduction of BDNF in the brain has been associated with Alzheimer's disease and depression, so increasing this growth factor with a common medication is exciting."

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