Alzheimer's-Like Memory Loss Reversed in Mice02/29/12
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
For more about
Alzheimer's disease, try the U.S. National Library of Medicine.
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