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.

Wednesday, August 20, 2025

Repairing the Aging Blood-Brain Barrier: Real Possibilities

 How long before your competent? doctor gets research going to determine the best intervention to fix your blood brain barrier damage from your stroke? Oh, your doctor PLANS ON DOING NOTHING? RUN AWAY!

The latest here:

Repairing the Aging Blood-Brain Barrier: Real Possibilities

study recently published in Nature has identified a key factor in the age-related breakdown of the blood-brain barrier (BBB) and has demonstrated that this damage may be reversible, potentially paving the way for new therapeutic strategies for neurodegenerative and cerebrovascular diseases, such as Alzheimer’s disease, Parkinson’s disease, and stroke.

The study, led by Sophia M. Shi, PhD, now a principal investigator at the Rowland Institute at Harvard but a PhD student at Stanford University during the study, focuses on the endothelial glycocalyx of the brain’s vasculature, also known as the brain’s “sugar shield.” This catchy moniker is given by the fact that the glycocalyx is a sugar-rich layer lining the luminal surface of endothelial cells in the brain vasculature.

photo of Sophia Shi, Ph.D
Sophia M. Shi, PhD

Composed of proteoglycans, glycoproteins, and glycolipids, the glycocalyx — literally meaning “sugar coat” — is the first point of contact between the blood and the vasculature of the entire body, assisting in cell adhesion, providing protection, and helping control the movement of fluids and molecules between the bloodstream and surrounding tissues.

It also plays a critical role in maintaining the integrity of BBB.

“This blood-brain barrier or vascular dysfunction is a really common hallmark in aging but also a lot of age-related diseases like Alzheimer’s disease, Parkinson’s disease, stroke,” Shi said. “We have these early changes in the vasculature that we can see.”

The research team demonstrated how a class of proteins of the glycocalyx known as mucin-domain glycoproteins is crucial for the barrier’s function, and its age- and disease-related decline is linked to a “leaky” BBB. The study showed how this decline can lead to brain hemorrhaging in mice.

photo of Lianchun Wang, MD
Lianchun Wang, MD

“There’s a lot of proteins from the brain, like IgG [immunoglobulin G] and fibronectins, that will be toxic for the neurons if they leak. For years, people have found that during aging, one of the major problems people have been vascular damage from leaking. So people think that’s one of the reasons to look at [this leaking and vascular damage] in neuroendocrine disease,” said Lianchun Wang, MD, professor of molecular pharmacology and physiology at the Morsani School of Medicine at the University of South Florida, Tampa, Florida. Wang was not part of the study.

The Stanford study was able to restore the integrity of the glycocalyx, improving the barrier’s function, reducing leaking, and reducing neuroinflammation and cognitive deficits in the mice.

“We really wanted to see if we could ameliorate aspects of pathology and cognitive function in disease models to make it more disease relevant and potentially translational,” Shi added.

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