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, September 21, 2015

A barrier against brain stem cell aging

We need something like this so send your doctor after how this can be used in humans.
http://loonylabs.org/2015/09/20/brain-stem-cell-aging/
Neural stem cells generate new neurons throughout life in the mammalian brain. However, with advancing age the potential for regeneration in the brain dramatically declines. Scientists now identified a novel mechanism of how neural stem cells stay relatively free of aging-induced damage. A diffusion barrier regulates the sorting of damaged proteins during cell division.


Yeast are good for making wine, bread, and brewing beer. But they are also a good model for neural stem cells in the mammalian brain. It was known that with every division cellular aging factors are asymmetrically distributed between the mother and the daughter cell, allowing for rejuvenation and full life span of the daughter independent of the age of the mother cell. At least partially responsible for this is the presence of a diffusion barrier that restricts movement of molecules from one side to the other side of the cell during cell division.
A group of scientists led by Sebastian Jessberger of the Brain Research Institute showed now that also the stem cells of the adult mouse brain asymmetrically segregate aging factors between the mother and the daughter cells. Responsible for this is a diffusion barrier in the endoplasmic reticulum (a channel system within the cell that is for example important for protein synthesis and transport).
The barrier prevents retention of damaged proteins in the stem cell daughter cell keeping the stem cells relatively clean.

“Neural stem cell divisions appear to be much more asymmetric than we had previously anticipated,” states Darcie Moore, postdoc in the group of Sebastian Jessberger and lead author of the study.

In addition, the authors of the new study found that the strength of the barrier weakens with advancing age. This leads to reduced asymmetry of damaged protein segregation with increasing age of the stem cell. This could be one of the mechanisms responsible for the reduced regeneration capacity in the aged brain as stem cells that retain larger amounts of damaged proteins require longer for the next cell division.

“This is an exciting new mechanism involved in stem cell division and aging. But as of now we are only just beginning to understand the molecular constituents and the true meaning of the barrier for stem cell division in the brain,” says Sebastian Jessberger.

One key question to be answered is whether the barrier is established in all somatic stem cells of the body. The answer to this question may open new routes to target age-dependent alterations of stem cell activity in human disease.
Sources:
Moore, D., Pilz, G., Arauzo-Bravo, M., Barral, Y., & Jessberger, S. (2015). A mechanism for the segregation of age in mammalian neural stem cells Science, 349 (6254), 1334-1338 DOI: 10.1126/science.aac9868

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