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, January 27, 2016

Study findings may help explain why risk of stroke changes after menopause

I hate these articles that don't link to actual research. You're on your own here unless you think your doctor will be useful.
http://www.news-medical.net/news/20160120/Study-findings-may-help-explain-why-risk-of-stroke-changes-after-menopause.aspx

Risk of stroke in women may come down to a compound the body produces from estrogen known as 2-methoxyestradiol (2-ME). Furthermore, the compound's therapeutic potential may extend beyond treating stroke in women to healing brain injuries in men, a new study in American Journal of Physiology—Endocrinology and Metabolism reports.
Microglia, the immune cells of the brain, maintain the brain and protect it from infection by consuming damaged cells and bacteria—a process called phagocytosis—and releasing toxic molecules to induce injured cells and bacteria to die. The same processes help "clean up the mess" after brain injury, such as after stroke or a head impact, says Edwin Jackson, PhD, of the University of Pittsburgh and the study's collaborating investigator. However, overactive microglia may kill brain cells that otherwise would have survived the injury, worsening instead of healing the damage, Jackson explains.
Mouse microglial cells exposed to 2-ME multiplied less and had reduced immune activity: 2-ME stopped phagocytosis and the release of toxic molecules by microglia. "2-ME prevented microglia from becoming overly active," Jackson says.
The findings help explain why risk of stroke in women changes after menopause. Menopause occurs when the ovaries stop producing the female sex hormones estrogen and progesterone. Prior to menopause, women have a lower risk of stroke compared to men. After menopause, women are at a higher risk. "Our study shows that microglia can metabolize (change) estradiol into 2-ME. So the female advantage before menopause may be in part the result of microglia making 2-ME from estradiol. Once estradiol levels collapse with menopause, the female advantage is lost. Administration of 2-ME could restore the female advantage," Jackson says. Estradiol is an estrogen and the primary female sex hormone.
The use of 2-ME is not limited to women. "Although 2-ME is derived from estradiol, 2-ME is not estrogenic and can be used in both women and men," Jackson notes. Because 2-ME "calms" microglia, it may be useful in treating or preventing other brain injuries including traumatic brain injury and chronic traumatic encephalopathy—the injury commonly found in professional football players and athletes in other contact sports, he says.
According to Jackson, current research on 2-ME supports that the compound is safe. "Unlike estradiol, 2-ME has anti-cancer activity, is cardio-protective and has beneficial activity in models of pulmonary artery hypertension. In fact, a slow-release formulation of 2-ME was developed and validated in a phase I clinical trial for pulmonary artery hypertension."
The next step is to corroborate 2-ME's effects, says Raghvendra Dubey of the University of Zurich and the study's lead investigator. These findings in cells "provide important leads which need to be further confirmed using in vivo (animal) models of brain injury," he says.

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