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But any application for humans remains years away, researchers stress
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.
For more about Alzheimer's disease, try the U.S. National Library of Medicine.
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