Don't get your hopes up too soon, it will probably take decades to get this to a therapy.
http://www.medpagetoday.com/Cardiology/Diabetes/33626
The widely used diabetes drug metformin might also offer a medical therapy for nervous system damage, researchers reported.
In
a series of experiments in culture and in animals, the drug promoted
the growth of new neurons, according to Freda Miller, PhD, of the
Hospital for Sick Children in Toronto, and colleagues.
And in a
classic behavioral test, mice treated with metformin formed new memories
faster that those given a control substance, Miller and colleagues
reported in the July 6 issue of Cell Stem Cell.
The
implication, they concluded, is that metformin or something like it
might be a "candidate pharmacological approach for nervous system
therapy" in such disorders as ischemic stroke and Alzheimer's disease.
Using
stem cells to create new neurons is an attractive therapy, but
approaches using either growth factors or small molecules have so far
not panned out, they noted.
Miller and colleagues had previously
showed that a molecule called CREB-binding protein, or CBP, was needed
for the best development of embryonic neural precursor cells. As well,
they showed that – to perform that task – CBP needed activation by
another molecule, atypical protein kinase C, or aPKC.
In liver
cells, they noted, the aPKC-CBP pathway is downstream of the AMP kinase
and is turned on by metformin, which activates the AMP kinase.
Miller
and colleagues hypothesized that metformin might activate the aPKC-CBP
pathway in neural stem cells, thereby creating new neurons.
In a
series of experiments in culture, they showed that, in fact, metformin
treatment promotes neurogenesis, both in mouse and human neural stem
cells.
In one experiment in mice, for example, metformin nearly
doubled the number of new neurons produced by stem cells, compared with
controls, a difference that was significant (P<0.05).
In
living mice, 12 days of metformin increased the number of new neurons
in the hippocampus – a region closely involved with the ability to make
new memories – by about 30%, compared with controls, Miller and
colleagues reported.
The process required normal levels of CBP; in animals with only one gene for the protein, metformin had no effect.
In
the key experiment, mice were forced to learn the position of a
platform hidden under the surface in a water-filled maze and then asked
rapidly to learn a new position.
Mice were injected with 200
milligrams per kilogram of metformin or with saline for 38 days; on days
22 through 38, they learned the initial position of the platform, which
provided an escape from the water-filled maze.
Then the platform was moved to the opposite quadrant of the maze, and the animals were asked again to learn its position.
In both tasks, the mice learned the platform positions with equivalent speed.
But
when they were put back in the maze – this time with the platform
removed -- control mice spent more time searching for it in the
original quadrant, while the metformin-treated animals preferentially
looked in the new region (P=0.05 and P=0.04, respectively).
Both groups of animals spent the same amount of time looking in the other two quadrants, where the platform had never been.
The
implication, Miller and colleagues argued, is that metformin helped the
mice form their new memories of the second position. Analysis showed
that their enhanced ability was paralleled by an increase in the number
of newborn adult dentate gyrus neurons.
To confirm the link, the
researchers repeated the experiment, but this time the metformin mice
were also given a drug that selectively kills actively dividing cells,
such as neural precursor cells.
That combination blocked the effect of metformin on memory and also reduced the number of new neurons, they reported.
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