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, August 19, 2015

Brain Equation: Subtract Protein, Generate Myelin-making Cells

It's a very simple question. DO WE NEED MYELIN REPAIR POST-STROKE?
And I bet there is not a single person in the world who can answer that. We have no one or no organization to go to to answer these simple questions. It mentions generating stem cells so maybe this could be useful to us in other ways.

Brain Equation: Subtract Protein, Generate Myelin-making Cells


That’s the conclusion of University at Buffalo scientists after deleting from the adult brain a protein necessary for early development. They found that this deletion actually fosters the growth of cells that generate myelin, the important protective coating neurons need to function.
The research on lab animals, published in Stem Cells and Development on July 28, provides new insight into how critical brain cells are generated. The finding may lead to improved treatments for brain injury, demyelinating diseases, certain developmental diseases and brain tumors.
The UB researchers studied Nuclear Factor I X (NFIX), a transcription factor – a protein that turns genes on and off.
NFIX is required for normal development of the early brain and it’s known that losing NFIX before birth results in a number of rare human diseases, characterized by severe developmental and physiological defects.
However, the new study shows that the loss of NFIX is necessary at a certain point in order for some brain cells to develop normally.
“This paper is about the increase in oligodendrocytes, the myelin-making cells, that we discovered when we deleted NFIX from adult neural stem cells,” explained lead author Richard M. Gronostajski, Ph.D., professor in the UB Department of Biochemistry. “This is of interest because producing more oligodendrocytes could help prevent the damage to neurons that occurs in MS and other demyelinating diseases, such as Krabbe’s Disease.” He directs the Genetics, Genomics and Bioinformatics Graduate program in the UB School of Medicine and Biomedical Sciences and UB’s Western New York Stem Cell Culture and Analysis Center (WNYSTEM).
Gronostajski’s lab is at UB’s New York State Center of Excellence in Bioinformatics and Life Sciences and he is also a professor at Roswell Park Cancer Institute.
Thirty years ago, while working in a lab at Albert Einstein College of Medicine, he contributed to the discovery of NFI proteins. His new research demonstrates how complex a role NFIX and other related transcription factors play in development.
He explained that oligodendrocytes surround neurons, which transmit electrical signals in the brain, protecting them from damage and speeding the transmission of those signals.
The research shows that as neural stem cells differentiate into oligodendrocytes, the expression of NFIX decreases, apparently an essential step in the normal formation of the myelin-making cells.
“In terms of a treatment, this could lead to the development of a small molecule that could be used to shut off NFIX activity in MS patients, thus promoting the growth of more oligodendrocytes,” explained Gronostajski.
This study and previous ones have found that loss of NFIX could also increase the growth of adult neural stem cells, which, in turn, generate new neurons in adult animals.
“This could also help us find ways to stimulate new neuron production in diseases where neurons die, such as in Alzheimer’s and Parkinson’s diseases and in spinal cord injury,” he said.
The researchers’ next step is to learn which genes are regulated by NFIX, and the best way to promote this increase in both oligodendrocytes and neural stem cells.
The work was funded by NYSTEM contracts, National Health and Medical Research Council project grants and the Australian Research Council Future Fellowship.
Source: University at Buffalo

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