Genetic Mutation Boosts Memory
Thursday, April 5, 2007; 12:00 AM
THURSDAY, April 5 (HealthDay News) -- Canadian researchers have discovered a gene mutation that actually improves long-term memory and could eventually lead to a memory-enhancing pill.
Working with mice, lead researcher Mauro Costa-Mattioli, a postgraduate fellow at McGill University in Montreal, and colleagues found that rodents that had a defective version of a gene that produces a memory-blocking protein could learn and remember tasks faster than normal mice.
"We discovered a protein that is called eIF2a that, when mutated, mice have an enhanced memory," Mattioli said. "We hope that this could be a good target to develop a compound that will mimic this mutation, and we can enhance memory in humans," he said.
In one experiment, the mice were trained to swim to a hidden platform. After several days of training, the mice with the gene mutation were able to find the platform significantly faster than normal mice, Mattioli said.
Mattioli likened it to reading pages of a textbook -- for most people, it might take several times to memorize everything. "But if a human had the same mutation, one would be able to remember it after one reading," he said.
To confirm that this gene mutation actually improved memory, the researchers treated the mutant mice with a molecule that increased the concentration of the memory blocker. When concentration of the memory-blocker was increased, the mice showed signs of memory impairment, Mattioli said.
The findings are published in the April 6 issue of the journalCell.
Mattioli thinks that finding a way to get the same memory-enhancing effect in humans could benefit patients with memory loss, including Alzheimer's patients. "We wouldn't cure Alzheimer's, but, hopefully, we can rescue the memory deficit, which is associated with the disease," he said.
One expert thinks this discovery could be important in understanding memory loss in Alzheimer's disease.
"Many researchers are pursuing the hypothesis that memory loss in Alzheimer's disease is caused by defects in the complicated machinery controlling the formation of synapses -- the critical connections between nerve cells that define functional circuits," said Greg M. Cole, associate director of the UCLA Alzheimer's Disease Research Center, and a professor of medicine and neurology at the University of California, Los Angeles.
"The authors have added a fresh insight into one of the pathways that make new proteins for forming new long-term memories." Cole said. "How this pathway relates to diseases like Alzheimer's with loss of synapses and memory remains to be seen, but it is easy to guess that it could."
To learn more about memory loss, visit the U.S. National Institute on Aging.
SOURCES: Mauro Costa-Mattioli, Ph.D., senior postgraduate fellow, McGill University, Montreal, Canada; Greg M. Cole, Ph.D., associate director, UCLA Alzheimer's Disease Research Center, and professor, medicine and neurology, University of California, Los Angeles; April 6, 2007,Cell