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, March 12, 2026

Irisin reduces neurodegeneration and neuroinflammation in the 6-hydroxydopamine rat model of Parkinson’s disease

 

Didn't your competent? doctor tell you about this a long time ago? Some human research already exists;  AND YOUR INCOMPETENT? DOCTOR DOESN'T KNOW ABOUT IT?


Do you prefer your doctor and hospital incompetence NOT KNOWING? OR NOT DOING?

 

  • irisin (12 posts to October 2013)

Irisin reduces neurodegeneration and neuroinflammation in the 6-hydroxydopamine rat model of Parkinson’s disease


https://doi.org/10.1016/j.brainresbull.2026.111814Get rights and content
Under a Creative Commons license
Open access

Highlights

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    Irisin, an exercise-induced myokine, is neuroprotective in a Parkinsonian rat model.
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    Irisin alleviated motor impairment in the 6-hydroxy-dopamine Parkinson rat model.
  • •
    Microglial/astrocytic morphological changes are attenuated by intracerebral irisin.

Abstract

Parkinson’s disease (PD) is a progressive neurodegenerative disorder that affects millions of individuals worldwide. With the number of cases expected to continue rising, there is an urgent need for new treatments. Irisin, a peptide released by skeletal muscle during exercise, has been proposed as a key mediator of the beneficial effects of physical activity on the brain. However, its potential neuroprotective role in PD remains unclear. Here, we established a PD model by injecting 6-hydroxydopamine into the right striatum of rats, followed by irisin administration into both cerebral lateral ventricles. Motor behavior was assessed, and brain tissue was collected for analysis of nigral dopaminergic neuron numbers in the substantia nigra pars compacta (SNc), axonal terminal density in the striatum (CPu), and glial cell reactivity. Our findings showed that irisin-treated PD animals exhibited a higher number of dopaminergic neurons (n = 6/group; +11,8 ± 3,6%; p = 0.013), increased terminal density in the striatum (n = 6/group; +18,8 ± 5,1%; p < 0.001), and reduced the number of asymmetrical rotations when compared to untreated rats (n = 6/group; −73,6 ± 32,4%; p < 0.001). Additionally, irisin reduced microglia (n = 6/group; SNc: −27.8 ± 4.5%; p = 0.030; CPu: −25.1 ± 2.8%; p = 0.019) and astrocytes (n = 6/group; SNc: −30.9 ± 5.3%; p = 0.013; CPu: −55.0 ± 7.5%; p < 0.001) density and alleviated morphological alterations (n = 30 cells/group; increased number of branches and endpoints of glia cells; p < 0.01 in all cases) indicating an anti-inflammatory effect. These results suggest that irisin exerts neuroprotective and anti-inflammatory effects in the 6-hydroxydopamine rat model of PD, highlighting its potential as a promising tool in the management of PD.
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