Never mind, more study is needed which will never occur under the current fucking failures of stroke associations. Unless you can personally fund researchers to find the answer All these possibilities and NO ONE is following up them to actually help stroke survivors.
http://medicalxpress.com/news/2016-07-astrocytes-mitochondria-neurons.html
A combined team of researchers from
Massachusetts General Hospital/Harvard Medical School in the U.S. and
Xuanwu Hospital, Capital Medical University in China has found that when
neurons in the mouse brain suffer mitochondrial damage astrocytes
donate some of their own to help repair them. In their paper published
in the journal Nature, the team describes how they conducted a
series of tests designed to find out whether astrocytes donate
mitochondria material and if so, whether it helps to restore health to
damaged neurons.
Astrocytes are
star-shaped glial cells that surround neurons, providing insulation and
support—prior studies have shown that they are involved in carrying out
removal of dead material. In this new effort, the researchers started
with the results of experiments conducted by a team at Columbia
University four years ago that showed that bone marrow stem cells
provided mitochondria to damaged lung cells to help them recover—they wanted to know if the same might be true for astrocytes and neurons.
To find out, the researchers engineered mice to produce extra amounts
of a signaling enzyme called CD38. They then found that when rodent
astrocytes were mixed with them, they expelled some degree of
mitochondrial material—neurons added to the mix were then found to
absorb some of the mitochondrial material.
The next step was to find out if the same process actually happened
in a living animal. They found that it did by causing brain injuries to
mice and then injecting the sites with mitochondria they had retrieved
from astrocytes—microscopic
analysis showed the neurons had, indeed, absorbed the material and that
as a result, the neurons were healthier than were injured cells that
had not received injections.
The researchers also wanted to know if CD38 signaling was necessary
for the process to work—to find out, they injected material that
interfered with its function into test mice—those with such injections
were found to have less astrocyte-donated mitochondrial material in
their neurons than did those that did not receive such injections, which suggest that it is a necessary part of the process.
The overall results by the team suggest that human stroke patients
might benefit from CD38 injections or drugs that cause the body to
produce it, but the researchers are quick to point out that the protein
is very active throughout the body, which means such therapies could
cause a large number of unknown side effects. More study is needed, but
the findings do offer hope for treating such injuries and perhaps
maladies such as Parkinson's disease.
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