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
No comments:
Post a Comment