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, June 11, 2013

Research Shows Tocomin® May Improve Stroke Outcome - alpha-tocotrienol

Ok, but the mouse inflammation model does not match the human model. Everyone in stroke research should know that. And it's concerning that they are testing a commercial product. The previous studies showed that you had to have a certain level of this in your system prior to your stroke to help.


Research Shows Tocomin® May Improve Stroke Outcome - alpha-tocotrienol

New findings show alpha-tocotrienol may lead to improved stroke outcome by protecting neurons from cell death, according to a study published in the Journal of Cerebral Blood Flow and Metabolism.
Tocomin® from Carotech, the alpha-tocotrienol used in the study, is a 12-Lox inhibitor that acts to confer neuroprotection post-stroke. A team of researchers at The Ohio State University Wexner Medical Center elucidated the mechanisms of microRNA precursor (miR29) in stroke-induced neuronal injuries. They showed that alpha-tocotrienol prevented miR29 loss at the infarct site during stroke.
 “Micro RNAs (miR) are small non-coding RNA molecules that play important role in regulating gene expression at the translation level, and miR29 is the micro RNA in the study of stroke etiology and in many other neurodegenerative disorders including Alzheimer’s Disease," said Savita Khanna, co-researcher of the study.
The miR29 family of genes, miR29a, miR29b1, miR29b2 (collectively miR29b) and miR29c, plays an important role in regulating gene expression. MiR29b is recognized as a neuronal survival factor. Specific loss of miR-29b at the infarct site after stroke leads to neuronal cell death. Prevention of such stroke-induced loss of miR-29b significantly improves stroke outcomes.
Researchers used the mouse stroke model, where mice were subjected to temporary middle-cerebral artery occlusion (MCAO), to induce stroke. At 48 hours after MCAO, there was a significant loss of miR29b at the infarct site.
Re-introducing miR29b at the infarct site decreased stroke-induced brain lesion by half compared to the control. In addition, the miR29b significantly improved post-stroke sensorimotor functions, where the cohort receiving miR29b had better agility and movement 48 hours post-stroke compared to control.
Then, researchers tested the efficacy of alpha-tocotrienol in the same mouse stroke model. Test mice were given 50 mg/kg body weight of alpha-tocotrienol and control mice were given vitamin E-stripped corn oil for 10 weeks before subjecting them to MCAO. The results showed that stroke-induced loss of miR29b was completely spared in the tocotrienol supplemented group, which resulted in smaller lesion size.
“I am excited with this new fifth checkpoint of tocotrienol in preventing stroke-induced injuries," said WH Leong, vice president of Carotech."It further strengthens the science of Tocomin® for neuroprotection. In a stroke event, neuroprotective miR29b is loss due to the downstream product of 12-Lipoxygenase (12-Lox) called 12HETE, which leads to neuronal cell death. Tocomin® is able to rescue miR29b by inhibiting 12-Lox."

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