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.

Saturday, July 18, 2026

Researchers Prolong Brain Healing Window Post-Stroke

 Do your really think your incompetent? doctor and hospital will get further research going on this? Then you're living in la-la land!

Of course, just to prove the point your incompetent? doctor did nothing with all this earlier IGF-1 research!

Your fuckingly incompetent? doctor DID NOTHING WITH ALL THIS EARLIER RESEARCH! And you still see them?

IGF-1 (21 posts to March 2014)

Researchers Prolong Brain Healing Window Post-Stroke

Blocking the activity of ZFP384 can prolong the brain’s endogenous repair functions after stroke, report researchers in a collaborative study. They developed an antisense oligonucleotide-based therapy that sustained the reparative activity of microglia by promoting remyelination and neural plasticity, thereby improving functional recovery in mice. Surprisingly, these results were observed even when the treatment began weeks after injury. The findings reveal a promising strategy to extend the brain’s recovery window after stroke, improving long-term outcomes.


Stroke is one of the leading causes of long-term disability worldwide, which often results in impairments in movement, speech, and cognition in patients. While rehabilitation helps patients regain some lost functions, the brain’s natural ability to repair itself often fades within a few months after an injury. This limited period of spontaneous recovery poses a major challenge for patients, often resulting in permanent neurological deficits after the brain’s intrinsic repair capacity declines. Although this loss of reparative ability has been studied extensively, the mechanism behind this loss remains unclear.


To uncover the reason why this happens, a team led by Assistant Professor Jun Tsuyama and Professor Takashi Shichita from the Department of Neuroinflammation and Repair, Institute of Science Tokyo (Science Tokyo), Japan, conducted research in collaboration with researchers from the Tokyo Metropolitan Institute of Medical Science, Kyushu University, Japan, and the University of Freiburg, Germany. Their findings were published in the journal Nature on May 13, 2026.

After a stroke, the brain launches a coordinated repair program that involves several types of cells. Among these, microglia, the brain’s resident immune cells, play a pivotal role. Immediately after an injury, microglia are activated to trigger inflammation, but thereafter, they rapidly transition into a reparative state and produce growth factors, such as insulin-like growth factor 1 (IGF1), which support remyelination, strengthen neural connections, and promote functional recovery. But this only lasts for two months, limiting the brain’s capacity to repair further.

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