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.

Friday, March 7, 2025

Ghrelin promotes neurologic recovery and neurogenesis in the chronic phase after experimental stroke

 So, I guess your doctor was totally fucking incompetent in not creating protocols on ghrelin over a decade ago. You need to demand the hospital president FIRE SUCH INCOMPETENCY!

  • ghrelin (3 posts to February 2013)
  • Ghrelin promotes neurologic recovery and neurogenesis in the chronic phase after experimental stroke

    Abstract

    Background

    The neuroprotective and proangiogenic potential of ghrelin in acute ischemic stroke has been demonstrated in experimental studies. However, the transferability of these results is limited as ghrelin was administered either before or very early after stroke onset and follow-up was limited to the first days after stroke. The aim of this study was therefore to close and extend this knowledge gap. To this end, we investigated the effect of ghrelin in two different translational animal models, one investigating acute and one investigating long-term structural and functional recovery after experimental stroke.

    Methods

    Middle cerebral artery occlusion (MCAO) or photothrombotic stroke was induced in 65 adult male Wistar rats. Eleven sham-operated animals served as controls. The rats were treated with either ghrelin, the ghrelin receptor antagonist [D-Lys]-GHRP-6 or a control substance. Up to four weeks after ischemia, behavioral tests such as the cylinder test, the tape removal test, and the rotarod test were performed to examine sensorimotor deficits, and the Morris water maze was performed to examine effects on the acquisition and consolidation of new memories. The structural outcome was determined by a differential analysis of neurogenesis in relation to survival and proliferation of newborn neurons in the post-ischemic brain, angiogenesis and determination of infarct size.

    Results

    Ghrelin treatment improved motor and somatosensory functions and preserved the consolidation of new memories after photothrombotic stroke. As a structural correlate, long-term survival and sustained proliferation of neuronal cells after stroke was significantly increased in ghrelin-treated rats, while angiogenesis remained unaffected. In contrast to these neuroregenerative mechanisms, ghrelin did not induce immediate neuroprotective effects after MCAO.

    Conclusions

    Our results suggest that ghrelin has a significant pro-neuroregenerative effect by enhancing long-term survival and sustained proliferation of neurons in the dentate gyrus and peri-infarct area, thus promoting functional recovery. Overall, ghrelin represents a promising target in the subacute and chronic phase after ischemic stroke.

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