Researchers Find an Epigenetic Culprit of Memory Decline

In a mouse model of Alzheimer’s disease, memory problems stem from an overactive enzyme that shuts off genes related to neuron communication, a new study says.When researchers genetically blocked the enzyme, called HDAC2, they ‘reawakened’ some of the neurons and restored the animals’ cognitive function. The results, published February 29, 2012, in the journal Nature, suggest that drugs that inhibit this particular enzyme would make good treatments for some of the most devastating effects of the incurable neurodegenerative disease.“It’s going to be very important to develop selective chemical inhibitors against HDAC2,” says Howard Hughes Medical Institute investigator Li-Huei Tsai, whose team at the Massachusetts Institute of Technology performed the experiments. “If we could delay the cognitive decline by a certain period of time, even six months or a year, that would be very significant.”Read more at...HHMI News, February 2012.