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, November 3, 2014

Human Cells Model Alzheimer’s Disease

And if we had anything approaching a decent stroke association we would have a headline of 'Human Cells Model Stroke Neuronal Death Cascade'. But we don't because all they seem to do is write press releases. GAH!!!!!!!
http://www.nih.gov/researchmatters/november2014/11032014alzheimer.htm
Alzheimer’s disease is an irreversible, progressive brain disorder. It’s the most common cause of dementia among older people, affecting more than 5 million Americans. The condition, which isn’t a normal part of aging, slowly destroys memory and thinking skills.
Modified human neural stem cells form beta-amyloid plaques (red) in a 3-D gel culture system. Image by the researchers, courtesy of Nature.
Alzheimer’s disease has 2 key features in brain tissue: plaques and tangles. The plaques are abnormal clumps of toxic fragments of the protein beta-amyloid. These fragments are made from amyloid precursor protein and are found in the space between nerve cells. Tangles are abnormal masses of twisted protein threads inside cells made mainly of a modified form of the protein tau. This protein usually has a certain number of chemical tags, known as phosphate groups, attached. In Alzheimer’s disease, too many phosphate groups are attached. The tangles disrupt processes in cells, causing them to die.
To better understand the link between plaques and tangles, a team led by Drs. Rudolph Tanzi and Doo Yeon Kim at Massachusetts General Hospital used a cell culture system to develop a model of Alzheimer’s disease. The research was funded in part by NIH’s National Institute on Aging (NIA) and National Institute of Mental Health (NIMH). The study appeared online on October 12, 2014, in Nature.
The scientists grew human neural stem cells in a 3-D gel culture system. The cells were modified to produce high levels of 2 proteins—beta-amyloid precursor protein and presenilin—with mutations seen in inherited forms of Alzheimer’s disease. Over time, the neural cells secreted beta-amyloid, which formed plaques in the gel matrix. The cells also produced high levels of modified tau, which formed threads in the 3-D culture.
The team found that when they blocked beta-amyloid formation, plaques didn’t develop and levels of the modified tau protein decreased. This indicated that beta-amyloid accumulation contributes to the formation of tangles. When they added a compound that prevents extra phosphate groups from attaching to tau, it prevented the formation of tau tangles, even when amyloid plaques were present.
“In this new system that we call ’Alzheimer’s-in-a-dish,’ we’ve been able to show for the first time that amyloid deposition is sufficient to lead to tangles and subsequent cell death,” Tanzi says.
The cell culture system could potentially be used to screen drugs to prevent or treat Alzheimer’s disease. It might also inform development of cell culture models to study other neurodegenerative disorders.

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