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, December 22, 2016

Perlecan Domain V Therapy for Stroke: A Beacon of Hope?

Almost 6 years and there is only one human followup I can find.
The rodent testing from 2011 here: In 24 hours sounds pretty good.
https://www.jci.org/articles/view/46358
When systemically administered 24 hours after stroke, domain V was well tolerated, reached infarct and peri-infarct brain vasculature, and restored stroke-affected motor function to baseline pre-stroke levels in these multiple stroke models in both mice and rats.

Perlecan Domain V Therapy for Stroke: A Beacon of Hope?

The sad reality is that in the year 2012, people are still dying or suffering from the extreme morbidity of ischemic stroke. This tragedy is only compounded by the graveyard full of once promising new therapies. While it is indeed true that the overall mortality from stroke has declined in the United States, perhaps due to increased awareness of stroke symptoms by both the lay public and physicians, it is clear that better therapies are needed. In this regard, progress has been tremendously slowed by the simple fact that experimental models of stroke and the animals that they typically employ, rats and mice, do not adequately represent human stroke. Furthermore, the neuroprotective therapeutic approach, in which potential treatments are administered with the hope of preventing the spread of dying neurons that accompanies a stroke, typically fail for a number of reasons such as there is simply more brain matter to protect in a human than there is in a rodent! For this reason, there has been somewhat of a shift in stroke research away from neuroprotection and toward a neurorepair approach. (What goddamn wimps, just because something is hard is no reason to run away)This too may be problematic in that agents that might foster brain repair could be acutely deleterious or neurotoxic and vice versa, making the timing of treatment administration after stroke critical. Therefore, in our efforts to discover a new stroke therapy, we decided to focus on identifying brain repair elements that were (1) endogenously and actively generated in response to stroke in both human and experimental animal brains, (2) present acutely and chronically after ischemic stroke, suggesting that they could have a role in acute neuroprotection and chronic neurorepair, and (3) able to be administered peripherally and reach the site of stroke brain injury. In this review, I will discuss the evidence that suggests that perlecan domain V may be just that substance, a potential beacon of hope for stroke patients.
Keywords: Stroke, perlecan, neurogenesis, angiogenesis, neuroprotection, astrogliosis
Having a stroke, or any brain injury for that matter, has the potential to rob us of what makes us uniquely human. Whether the injury causes unilateral weakness, an inability to speak or process language, or other severe morbidity, the final outcome can profoundly reduce one’s quality of life. Despite this sobering reality, our tools to combat ischemic stroke, that kind of stroke caused by the blockage of a cerebral blood vessel (typically from a blood clot/thrombus), are very limited. If a stroke patient is “lucky” and they are quickly attended to in a capable hospital environment, they may receive tissue plasminogen activator (tPA) within a limited therapeutic window, measured in hours, in an attempt to bust the blood clot causing the stroke, re-establish blood flow to the affected brain area (which is not without its own risks of reperfusion injury1,2), and potentially have a good outcome. More recently, it has been demonstrated that tPA administered after a so-called “wake-up” stroke, where a patient has had a stroke while asleep and wakes up with stroke symptoms, may be efficacious even when the exact time of stroke onset cannot be pinpointed (the patient was asleep after all when the stroke occurred!).3 Of course, tPA is only effective if one suffers a stroke due to a thrombus, which is the case about 85% of the time, the remainder being due to bleeding in the brain (hemorrhagic stroke), thereby necessitating that health care providers prove the type of stroke, ischemic versus hemorrhagic, before tPA can be administered. Furthermore, tPA carries the risk of so-called “hemorrhagic transformation”, that is, causing a brain bleed, with potentially lethal consequences (the risks and benefits of tPA therapy for ischemic stroke are nicely reviewed in ref (4)). Finally, for exceptionally large clots that tPA would not be able to completely lyse or when the therapeutic window for tPA is missed, the option to mechanically retrieve the clot is often available (review in ref (5)). Again, this runs the inherent risk of reperfusion injury in a patient that is already hemodynamically unstable. Clearly, additional and better stroke treatment options are needed.
 

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