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, September 6, 2013

Effect of a single intrastriatal rotenone injection on oxidative stress and neurodegeneration in the rat brain

I'm not sure I'd want a pesticide injected into my brain even if nitric oxide and CoQ10 increased. But ask your doctor what they think about it. Most of us received rat poison(warfarin) so its not out of the question.

http://link.springer.com/article/10.1007/s00580-013-1807-4

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Abstract

We investigated the effect of a single injection of rotenone into the striatum on the development of oxidative stress, nigrostriatal cell injury and motor alterations in rats. Rotenone (1, 3, 5 and 9 mM; 5 μL/rat) or the vehicle (dimethyl sulfoxide) was injected into the right striatum. Control rats received the vehicle only. Rats were allowed to recover from the operation and were tested for behavioural changes on 7th and 30th days after rotenone injection. Biochemical markers of oxidative stress including malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide, paraoxonase 1 (PON1) activity and Q10 enzyme as well as monoamine neurotransmitters in the brain were determined after 30 days of rotenone treatment. Histopathology and tyrosine hydroxylase immunohistochemistry were also performed. Results: Intrastriatal injection of rotenone at 9 mM caused immediate death of rats. No mortality was observed with the lower concentrations of the pesticide. Rotenone at 1–5 mM resulted in increased brain oxidative stress in a dose-dependent manner. MDA increased by 23.5–64.9 %, while GSH decreased by 20.4–24.1 % in the contralateral cerebral hemisphere. Nitric oxide increased by 20.2–41.7 % in ipsilateral cortex. PON1 activity decreased by 12.5–38.2 % in ipsilateral cerebral cortex and by 31.2–65.3 % in ipsilateral striatum, respectively, but coenzyme Q10 increased in the ipsilateral cortex by 21–26.3 %. There was decreased dopamine and serotonin in the ipsilateral striatum after rotenone injection. Tyrosine hydroxylase immunoreactivity was markedly decreased in ipsilateral substantia nigra in the rotenone-treated in contrast to the vehicle-treated rats. Rotenone increased the number of degenerated cells in substantia nigra in a dose-dependent manner. It also caused depletion of pigment granules from cells. Degenerative changes were also observed in the contralateral hippocampus and cortex especially after the highest dose of rotenone. The number of spontaneous rears made during 30 min in the cylinder was decreased in both limbs; the decrease being more evident in the ipsilateral side. Thus, a single intrastriatal injection of rotenone (a) caused a significant nigrostriatal degeneration and loss of dopamine and serotonin from the striatum; (b) elicited cell degeneration in the hippocampus and cortex; (c) induced oxidative stress and neuronal injury (this latter effect of rotenone was not region specific); and (d) the motor deficits (decreased rearing activity) occurred in both limbs

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