They found that when the functions of normal CBP is suppressed in adult rodents, the animals had trouble forming long-term memories, suggesting that CBP is required for the formation of long-term memory and that defects in CBP are involved in cognitive dysfunction.
Furthermore, the scientists found that they were able to correct this defect by administering a drug that restored CBP's function.
"This is significant," says Mark Mayford, Ph.D., an associate professor of cell biology and a member of the Institute for Childhood and Neglected Diseases at Scripps Research. Before moving to Scripps Research four years ago, Mayford was a faculty member at UCSD, where together with another UCSD scientist Edward Korzus, Ph.D., they initiated the research.
"There is a link between this molecule and very severe problems in humans," Mayford added, noting that the findings may be significant for children with the rare but severe developmental disorder known as Rubinstein-Taybi syndrome, which causes growth and mental retardation and several anatomical abnormalities. These children have mutations in their CBP genes.
Scientists have long known that when laboratory animals are treated with a class of drugs known as protein synthesis inhibitors, which stops the production of proteins in the animals' brains, these animals lose their long-term memory. This observation has led scientists to predict that the formation of long-term memory requires new protein synthesis.
This prediction has since been borne out in experiments repeated in many different species -- from mice to fruit flies.
Contact: Jason Bardi
Scripps Research Institute