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, October 7, 2026

Human dental pulp stem cell secretome boosts stroke recovery

And your incompetent? doctor DID NOTHING with this earlier secretome research, right?

Complex "cocktail" in white blood cells has regenerative effect after heart attack or stroke December 2015

The massive incompetence of the complete stroke medical world is mind boggling! 

The latest here:

 Human dental pulp stem cell secretome boosts stroke recovery

Ischemic stroke can leave lasting neurological damage after the initial vascular event, with oxidative stress, neuroinflammation, neuronal death, and disruption of neural connectivity contributing to impaired recovery. Although current interventions provide partial protection, their ability to prevent delayed neuronal injury remains limited, highlighting a major barrier to functional recovery.

The human dental pulp stem cell (hDPSC) secretome contains extracellular vesicles, growth factors, antioxidant enzymes, and immunomodulatory proteins and may offer a potential cell-free therapeutic approach. However, understanding of their therapeutic impact on delayed neuronal injury after reperfusion is limited.

Now, a study led by Professor Won-Jae Kim from the Stem Cell Secretome Research Center, Department of Oral Physiology, School of Dentistry, Chonnam National University, South Korea, investigated whether the hDPSC secretome could improve functional recovery in a photothrombotic mouse model and examined the biological processes associated with its effects. Their study was made available online on July 23, 2026, in the journal Advanced Science.

By utilizing the bioactive factors secreted by stem cells rather than the cells themselves, secretome-based therapy overcomes the classic hurdles of cell transplantation, such as poor cell survival, immune rejection, and tumorigenesis. We wanted to investigate if the hDPSC secretome could be deployed as a safe, supportive treatment to mitigate secondary brain injury, modulate neuroinflammation, and accelerate neural repair post-stroke."

Professor Won-Jae Kim, Stem Cell Secretome Research Center, Department of Oral Physiology, School of Dentistry, Chonnam National University, South Korea

The study identified 299 proteins uniquely present in the hDPSC secretome, which were majorly associated with extracellular vesicles, immunomodulation, neuroprotection, angiogenesis, apoptosis regulation, and oxidative-stress resistance. Several of these proteins were particularly associated with antioxidant defense. While SOD2, GSR, and GSTP1 were tied directly to the brain's antioxidant defense network, proteins like GRN, CSF1, and LRP1 emerged as key regulators of microglial phenotype regulation.

The hDPSC secretome improved microglial cell viability, reduced oxidative stress, and restored mitochondrial function in the in vitro study. It restored expression of the mitochondrial fusion protein Mfn2 and antioxidant enzyme SOD1 while reducing hypoxia-associated HIF-1α expression. Additionally, hDPSC secretome suppressed microglial migration and inflammation, promoting a shift from the pro-inflammatory M1 phenotype toward the pro-healing M2 phenotype.

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