Alzheimer’s Memory Mice
March 1, 2012 by staff
Alzheimer’s Memory Mice, 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.”
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