NEW YORK (Reuters Health) - You've heard of research designed to uncover nuances of memory. Now, a new study sheds light on the processes mouse brains use to forget, findings that may one day help investigators understand why people experience memory loss as they age.

In experiments with mice, David Genoux of the Swiss Federal Institute of Technology in Zurich and his colleagues found that suppressing the activity of an enzyme known as protein phosphatase 1 (PP1) appeared to improve the mice's memory. This suggests that PP1 is actively involved in forgetting.

The brain's capacity for memory storage is likely limited, study author Dr. Isabelle M. Mansuy of the Swiss Federal Institute of Technology told Reuters Health, so it is perhaps to the advantage of mice to eliminate memories or prevent their formation to avoid brain "saturation." Figuring out how animals forget is an important aspect of determining how they remember, she added. "I think if we want to understand learning and memory deeply, we have to understand all of it," Mansuy said.

Mansuy and her team report their findings in the August 29th issue of the journal Nature.

The investigators discovered the importance of PP1 through a series of experiments using mice. Researchers have long known that animals remember best when learning sessions are punctuated with long rest intervals, rather than short ones.

During the experiments, the researchers presented mice with new objects for an extended period of time or in shorter blocks, then tested the mice to see if the objects had become familiar to them.

The authors confirmed that the mice remembered the objects better when they were presented to them during learning periods separated by longer, rather than shorter, intervals. They also found the mice learned better when the familiarization period was given as five 5-minute sessions, rather than a single 25-minute block.

The researchers then used a technique that enabled them to temporarily block the activity of PP1 in the mice, and repeated the memory tests. They found that without PP1 activity, the mice could remember just as well after the single, longer learning session as they could when taught in five shorter sessions. Therefore, according to Mansuy and her colleagues, when PP1 is active it somehow interferes with the formation of memories during uninterrupted learning periods.

In an accompanying article, Drs. Alcino J. Silva and Sheena A. Josselyn of the University of California in Los Angeles explain that PP1 inactivates a substance known as CREB, which, under normal circumstances, helps designate which genes should be used to form new proteins. Blocking the activity of CREB interferes with the formation of new proteins, which can cause memory problems, they note.

In an interview with Reuters Health, Mansuy said that age-related memory loss may consequently result from increases in PP1 over time. Although the reasons behind these increases remain unclear, the current findings may one day be used to help researchers understand memory loss that is not linked to a physical problem such as damage of the brain tissue.

However, she stressed that since the current findings were conducted in mice, they are not immediately applicable to humans, nor is the technique the investigators employed to temporarily reduce PP1 levels in the mice's brains. She added that the study was also not intended to provide otherwise healthy adults with a means for improving their memory.

"That's not our goal at all," she said.

SOURCE: Nature 2002;418:970-975, 929-930.

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