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.

Monday, June 25, 2018

Protective Effects of Brain Infarction by N-Acetylcysteine Derivatives

You likely want this followed up with human testing since acrolein is implicated in Parkinsons. That followup is your doctor and stroke hospitals responsibility. Not doing so is pure incompetency.

Researchers ID "Key Factor" in Development of Parkinson's

 

Parkinson’s Disease May Have Link to Stroke

 

Protective Effects of Brain Infarction by N-Acetylcysteine Derivatives

Takeshi Uemura, Kenta Watanabe, Kenta Ko, Kyohei Higashi, Noriyuki Kogure, Mariko Kitajima, Hiromitsu Takayama, Koichi Takao, Yoshiaki Sugita, Akihiko Sakamoto, Yusuke Terui, Toshihiko Toida, Keiko Kashiwagi, Kazuei Igarashi
https://doi.org/10.1161/STROKEAHA.118.021755
Stroke. 2018;49:1727-1733
Originally published June 4, 2018
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Abstract

Background and Purpose—We recently found that acrolein (CH2=CH-CHO) is more strongly involved in brain infarction compared with reactive oxygen species. In this study, we looked for acrolein scavengers with less side effects.
Methods—Photochemically induced thrombosis model mice were prepared by injection of Rose Bengal. Effects of N-acetylcysteine (NAC) derivatives on brain infarction were evaluated using the public domain National Institutes of Health image program.
Results—NAC, NAC ethyl ester, and NAC benzyl ester (150 mg/kg) were administered intraperitoneally at the time of induction of ischemia, or these NAC derivatives (50 mg/kg) were administered 3× at 24-h intervals before induction of ischemia and 1 more administration at the time of induction of ischemia. The size of brain infarction decreased in the order NAC benzyl ester>NAC ethyl estergt;NAC in both experimental conditions. Detoxification of acrolein occurred through conjugation of acrolein with glutathione, which was catalyzed by glutathione S-transferases, rather than direct conjugation between acrolein and NAC derivatives. The level of glutathione S-transferases at the locus of brain infarction was in the order of administration of NAC benzyl ester>NAC ethyl estergt;NAC>no NAC derivatives, suggesting that NAC derivatives stabilize glutathione S-transferases.
Conclusions—The results indicate that detoxification of acrolein by NAC derivatives is caused through glutathione conjugation with acrolein catalyzed by glutathione S-transferases, which can be stabilized by NAC derivatives. This is a new concept of acrolein detoxification by NAC derivatives.
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