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, April 23, 2018

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

You need to know about this because of your chance of getting Parkinsons. You can tell how incompetent your doctor and stroke hospital are by whether or not they even know they should be following this type of research. 

Parkinson’s Disease May Have Link to Stroke

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

A molecule has been identified that appears to play an important role in the development of Parkinson's disease, a debilitating disease that affects millions of people around the world.
The discovery could lead to therapies, potentially including drugs currently on the market, and it could facilitate earlier diagnosis and prevention of the neurological disorder.
It's a "good news, bad news, good news" development that bears watching.
First, good news: Researchers at Purdue University have identified a compound that accumulates in Parkinson's disease-affected brain tissue. The compound, acrolein, is a toxic, foul-smelling byproduct of burning fat (the brain uses fat for fuel) and is normally eliminated from the body. But the research team has found that the substance can promote the build-up of a protein called alpha-synuclein. When this protein accumulates in a region of the brain called the substantia nigra, it destroys the cell membranes and key machineries of neurons, killing these brain cells.
Dr. Riyi Shi, professor in the Department of Basic Medical Sciences, College of Veterinary Medicine and Weldon School of Biomedical Engineering, says that when this cell death becomes extensive enough, the symptoms of Parkinson’s disease becomes evident.
"Acrolein is a novel therapeutic target, so this is the first time it's been shown in an animal model that if you lower the acrolein level you can actually slow the progression of the disease," Shi says. "This is very exciting. We’ve been working on this for more than 10 years."
Jean-Christophe (Chris) Rochet, professor in the Department of Medicinal Chemistry and Molecular Pharmacology in the College of Pharmacy, and a co-investigator on the study, adds a cautionary note (this is the bad news).
“In decades of research, we've found many ways to cure Parkinson's disease in pre-clinical animal studies, and yet we still don’t have a disease therapy that stops the underlying neurodegeneration in human patients," he says. "But this discovery gets us further down the drug-discovery pipeline, and it's possible that a drug therapy could be developed based on this information."
Rochet says that in experiments using both animal models and cell cultures, the role of acrolein was confirmed.
"We've shown that acrolein isn’t just serving as a bystander in Parkinson's disease. It's playing a direct role in the death of neurons," he says.
The research is published in the April issue of the scientific journal Molecular and Cellular Neuroscience.

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