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.

Showing posts with label FSH hormone. Show all posts
Showing posts with label FSH hormone. Show all posts

Thursday, March 24, 2022

Blocking hormone in females improves Alzheimer’s symptoms in mice

With your excellent chance of getting dementia, you'll want your doctor to be following this closely. Do not self treat,

Your risks of dementia, has your doctor told you of this?

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018

Where are the  protocols to prevent your dementia?

The latest here:

 Blocking hormone improves Alzheimer’s symptoms in mice

At a Glance

  • Researchers found that a hormone called FSH can act on neurons in the brain and increase the production of proteins implicated in Alzheimer’s disease.
  • Blocking FSH reduced Alzheimer’s symptoms in mice, suggesting a new approach to developing treatments for the disease.
Illustration showing clumps of amyloid around a branched neuron In Alzheimer’s disease, amyloid beta plaques, shown here in orange, collect around neurons in the brain. Kateryna Kon / Shutterstock

Women are at greater risk than men for developing Alzheimer’s disease over their lifetimes. The disease also tends to get worse faster in women, and women experience a broader range of cognitive symptoms—those related to thinking, learning, and memory.

Researchers have been studying whether hormones play a role in these differences between the genders. A team led by Dr. Mone Zaidi from Mount Sinai and Dr. Keqiang Ye from Emory University has been examining the many roles a hormone called follicle stimulating hormone (FSH) plays in the body.

FSH levels rise sharply in women around the time of menopause. In previous work, the researchers found that blocking FSH in mice can prevent weight gain and reduce bone loss—two other common changes in women’s bodies during and after menopause.

In a new study, the team investigated whether FSH is involved in the development of Alzheimer’s. The work was funded in part by NIH’s National Institute on Aging (NIA). Results were published on March 2, 2022, in Nature.

The researchers first put mice engineered to develop Alzheimer’s disease into a menopausal state. Levels of FSH rose in the blood of these mice. They also had accelerated cognitive decline and a buildup of amyloid beta plaques and tau tangles in their brains, which are hallmarks of Alzheimer’s disease.

When the researchers gave the mice an antibody that blocked FSH, these effects were much less severe. Male mice, which produce some FSH, also had less amyloid beta build-up in the brain after treatment with the antibody.

Further experiments found that blocking FSH caused a reduction in certain enzymes called the C/EBPβ-AEP/δ-secretase pathway in neurons within the brain. This pathway contributes to both amyloid beta and tau buildup.

In addition to the work in mice, the team found receptors for FSH in tissue samples taken from human and rat brains. Further work showed that that FSH can cross the blood-brain barrier and bind to these receptors on nerve cells.

In both human and rat neurons, when FSH bound to these receptors, it activated the C/EBPβ-AEP/δ-secretase pathway and caused amyloid beta and tau production. Blocking these receptors in the brain with a different technique also decreased Alzheimer’s symptoms in mice.

The team further found that giving injections of FSH to both female and male mice engineered to develop Alzheimer’s accelerated development of the disease. In contrast, differing levels of estrogen, another hormone, didn’t affect the development of cognitive symptoms.

“We are excited and cautiously optimistic that the molecule FSH may play an important role in Alzheimer’s disease, bone loss, and obesity simultaneously,” Zaidi says.

The team has developed an antibody to block FSH in people and is now testing it for safety in animal models. They hope to eventually test it in clinical trials for the prevention of Alzheimer’s as well as bone loss and obesity.

—by Sharon Reynolds

Related Links

References: FSH blockade improves cognition in mice with Alzheimer's disease. Xiong J, Kang SS, Wang Z, Liu X, Kuo TC, Korkmaz F, Padilla A, Miyashita S, Chan P, Zhang Z, Katsel P, Burgess J, Gumerova A, Ievleva K, Sant D, Yu SP, Muradova V, Frolinger T, Lizneva D, Iqbal J, Goosens KA, Gera S, Rosen CJ, Haroutunian V, Ryu V, Yuen T, Zaidi M, Ye K. Nature. 2022 Mar 2. doi: 10.1038/s41586-022-04463-0. Online ahead of print. PMID: 35236988.

Funding: NIH’s National Institute on Aging (NIA), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), and National Institute of General Medical Sciences (NIGMS); Harrington Discovery Institute.