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March 1st, 2012 
FAKE NEWS for the Zionist agenda WEDNESDAY, Feb. 29 (HealthDay News) — New research in mice
suggests that Alzheimer’s disease triggers a protein that contributes to
the breakdown of the brain’s memory.
If the findings are confirmed in humans, they could solve part of the
puzzle of how gunk-like substances in the brain cause Alzheimer‘s disease
and lead to memory loss. It’s conceivable that a drug could be developed
to turn off the process and reverse memory problems — as the researchers
managed to do with mice.
For now, the research is in its early stages and it could take five to
10 years to get to drug experiments in humans, said study author Johannes
Graff, a postdoctoral researcher at Massachusetts Institute of Technology.
Even if a drug is developed using this knowledge, it would only treat the
symptoms of Alzheimer’s and not the root cause, he said.
But it could mark a major advance to be able to turn around the memory
problems spawned by Alzheimer’s, Graff said, adding, “We can show that
this is potentially reversible.”
There are more than 5 million Americans who have been diagnosed with
Alzheimer’s, according to the U.S. National Institute of Neurological
Disorders and Stroke (NINDS).
Researchers believe that Alzheimer’s disease begins when the brain
becomes clogged by substances known as beta-amyloid plaques and tau
tangles. The new research in mice, Graff said, suggests that when a
protein known as histone deacetylase 2 (HDAC2) is triggered, it shuts down
genes that are crucial to memory. By preventing the buildup of HDAC2 in
the brains of mice, the researchers were able to protect against memory
loss.
Brain tissue from deceased Alzheimer’s patients also showed higher
levels of HDAC2 in regions where memory and learning are known to be
located, the scientists added, and they theorized that the accumulation of
beta amyloid deposits in the brain may be what sends HDAC2 into
overdrive.
“If your memory is everything that you know written in a book, then in
order to have access, you have to open the book and to turn the pages,”
Graff said. In Alzheimer’s, “this mechanism actually closes your memory
book and makes the pages — the genes — inaccessible.”
The good news is that this latest research suggests that the “blockade”
is potentially reversible, Graff said. In other words, the book hasn’t
been destroyed. “We are proposing to reopen the book and allow it to be
more easily read,” he said.
There are caveats to the research, said Dr. Brad Dickerson, an
associate professor of neurology at Harvard Medical School.
“This is a very early basic science study in mice and requires
substantial additional investigation in order to determine whether it is
worth pursuing in patients,” he said. “The leap from animal studies to
human clinical trials is a big one and always takes many years. Drugs in
this class are being studied in various types of cancer, which hopefully
will provide an indication of their side effects and other important
information about how feasible it would be to give these types of
medications to patients with Alzheimer’s disease if further studies
support the potential value of this approach.”
Research like this is important, Dickerson added, because “we need
studies like this in animals to begin to prove the concept that new drugs
of this sort have potential.”
The study, which was funded by NINDS, appeared online Feb. 29 in the
journal Nature.
More information
For more about Alzheimer’s disease, try the U.S. National Library of
Medicine.
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