A new weapon against stroke: Stem cell study uncovers the brain-protective powers of astrocytes

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One of regenerative medicine's greatest goals is to develop new treatments for stroke. So far, stem cell research for the disease has focused on developing therapeutic neurons—the primary movers of electrical impulses in the brain—to repair tissue damaged when oxygen to the brain is limited by a blood clot or break in a vessel. New UC Davis research, however, shows that other cells may be better suited for the task.


Published July 23 in the journal Nature Communications, the large, collaborative study found that astrocytes—that transport key nutrients and form the blood- barrier—can protect  and reduce disability due to stroke and other ischemic .

"Astrocytes are often considered just 'housekeeping' cells because of their supportive roles to neurons, but they're actually much more sophisticated," said Wenbin Deng, associate professor of biochemistry and molecular medicine at UC Davis and senior author of the study. "They are critical to several brain functions and are believed to protect neurons from injury and death. They are not excitable cells like neurons and are easier to harness. We wanted to explore their potential in treating neurological disorders, beginning with stroke."

Deng added that the therapeutic potential of astrocytes has not been investigated in this context, since making them at the purity levels necessary for stem cell therapies is challenging. In addition, the specific types of astrocytes linked with protecting and repairing brain injuries were not well understood.

The team began by using a transcription factor (a protein that turns on genes) known as Olig2 to differentiate human  into astrocytes. This approach generated a previously undiscovered type of astrocyte called Olig2PC-Astros. More importantly, it produced those astrocytes at almost 100 percent purity.

The researchers then compared the effects of Olig2PC-Astros, another type of astrocyte called NPC-Astros and no treatment whatsoever on three groups of rats with ischemic brain injuries. The rats transplanted with Olig2PC-Astros experienced superior neuroprotection together with higher levels of brain-derived neurotrophic factor (BDNF), a protein associated with nerve growth and survival. The rats transplanted with NPC-Astros or that received no treatment showed much higher levels of neuronal loss.

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  1. Yes, the linked article also discusses the connection with Alzheimer’s.

    It’s an important issue given the forecasts for an Alzheimer’s pandemic in the near future.

    Pretty much all the major non-communicable diseases, including alzheimer’s and strokes, seem to be related, though sometimes inversely and not all that clearly. There’s occasionally reports based on epidemiology work that indicates experiencing one of them tends to be ‘protective’ against some of the others.

    If they are fundamentally the same disease, just with different outcomes, then It may become very important that these diseases manifest in 1 form rather than the other. E.g. the public health funding implications for an epidemic of heart attacks and strokes vs an epidemic of Alzheimer’s are very different. At present the most effective public health policy for an impending Alzheimer’s epidemic may be to promote cigarette smoking among the elderly.

    I think a key point in the above linked article is the protection these cells provide neurons against oxidative stress. Just about anything can go wrong in human physiology as a consequence of uncontrolled oxidative stress.

    There seems to be only a few potential approaches to this problem:

    1. Identify and reduce the major causes of oxidative stress.
    2. Identify and reduce the cause of why mechanisms that otherwise control oxidative stress sometimes fail.
    3. Identify and enhance other mechanisms that might mitigate oxidative stress.

    Option 2 is probably the same as option 1. i.e. the failure of mechanisms that otherwise successfully control oxidative stress might be just because those same mechanisms are also subject to the same excessive oxidative stress themselves. These mechanisms exist to control normal stresses, but not if they’re operating well outside their normal range of capabilities.

    Which leaves only option 3. – developing new mechanisms that might control oxidative stress.

    Reason is that option 1, of reducing the cause of oxidative stress ,would simply eliminate the problem. No sane person is willing to pay for not having a problem. It’s a reverse form of ‘tragedy of the commons’ in game theory. To justify personal expenditure of resources or obtain a profitable ROI on R&D investment there needs to be a problem that can only be solved by producing a patentable remedy in the form of some kind of treatment commodity or service.

    It may only be a matter of time before the economic unsustainability of the forecast public health implications leads to non-profit oriented investment in mitigation rather than cures amenable to pharmaceuticals production. There are some indications that simply removing a range of potential causes might also lead to a reversal in some of these diseases, at least in the early onset cases.

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