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.

Thursday, September 11, 2014

Investigation of Sox9 ablation on neuroplasticity and recovery after ishcemic stroke

Another research project for our great stroke association to tackle. Unless you really think your neurologist is smart enough to figure out how to accomplish this by themselves.
http://ir.lib.uwo.ca/etd/2338/


Bethany Robin Lenore Bass, The University of Western OntarioFollow
Room 447 Medical Science Building

Degree

Master of Science

Program

Anatomy and Cell Biology

Supervisor

Dr. Arthur Brown

Delay of Publication

1

Abstract

Neuroplasticity is a key factor in post-stroke functional recovery. A chief inhibitor of post-stroke neuroplasticity is the expression of chondroitin sulfate proteoglycans (CSPGs). Recent research has shown that the transcription factor SOX9 is responsible for upregulating the expression of CSPGs in the injured central nervous system. Accordingly, CSPG levels are significantly lower in mice with the Sox9 gene conditionally knocked out. The purpose of this study was to determine how Sox9 ablation affects neuroplasticity and recovery after stroke. Behavioural test results revealed that Sox9 KO mice exhibited significantly improved functional recovery after stroke compared to controls. This correlated with increased contralesional corticofugal plasticity in the Sox9 KO animals, as highlighted by tract tracing studies. An increase in one type of glutamatergic input marker (VGLUT1) was observed at the deafferented red nucleus of the Sox9 KO mice, but not at the denervated the cervical spinal cord ventral horn. Further investigation into the effects of Sox9 ablation on post-stroke neuroplasticity would be beneficial to determine the potential of Sox9 as a therapeutic target.

Recommended Citation

Bass, Bethany Robin Lenore, "Investigation of Sox9 ablation on neuroplasticity and recovery after ishcemic stroke" (2014). University of Western Ontario - Electronic Thesis and Dissertation Repository. Paper 2338.
http://ir.lib.uwo.ca/etd/2338
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