The key to memory


Which brain cells are chosen to store memory? And if some cells are damaged, can new memories be stored elsewhere in the brain?

Scientists may be a little closer to answering these questions with the discovery of a protein that appears to control which cells are designated to store new memories. The finding may one day help people with Alzheimer’s disease or other brain injuries, researchers believe.

The international research team, headed by Sheena Josselyn of Toronto’s Hospital for Sick Children, discovered the protein CREB which plays a key role for which neurons store new memories.

In the study, scientists implanted CREB into a virus and then injected it into laboratory mice in a region of the brain called amygdale that is associated with emotional memory.

The mice were then given several learning tests, including one in which they were given a mild foot shock when a tone was sounded. In the experiments that followed, the mice froze with fear when they heard the tone – without getting shocked – because they recalled the unpleasant sensation.

“We got a really lovely behavioural enhancement,” Josselyn told the Canadian Press. “If a cell is low in CREB, it is less likely to keep a memory. If the cell is high in CREB, it is more likely to store the memory.”

Alcino Silva, study co-author and a professor of neurobiology and psychiatry at the David Geffen School of Medicine at UCLA, said the research could have profound implications for human diseases like Alzheimer’s.

“What the study suggests is that CREB is like a tag that identifies certain cells as repositories for memory,” Silva said from Los Angeles.

“And it’s important that the brain separates memory. The brain is constantly funnelling memory to different sites, and what this study suggests is that CREB is one of those traffic controllers that says, ‘Don’t store here, why don’t you store it there,’ so we don’t confuse what you’ve just stored with what you are storing now.”

The hope is that CREB could be injected into a human brain damaged by Alzheimer’s or other neurodegenerative diseases or head trauma to redirect memory storage to healthy neurons, Silva said.

People with Alzheimer’s disease, for instance, lose not only long-established memory, but are increasingly unable to store new memories as brain cells die.

“The whole process of memory storage decays quickly,” Silva told CP. “So it is our hope that if we can develop strategies to direct memory to healthy cells, we may one day postpone the traumatic effects of Alzheimer’s disease until we can cure it.”

Scientists note that while such an approach is possible, it likely won’t be anytime soon. In fact, human testing of CREB injections isn’t expected for another decade.

“This is very much science fiction-like, it’s very much in the future,” said Silva. “But you know today’s science fiction is tomorrow’s medicine.”

The study, thought to be the first showing how memory is allocated in the adult brain, was published in the April 20, 2007 issue of Science.

Over 30 million North Americans suffer from some type of clinically recognized learning or memory disorder, from inherited forms of mental illness to the gradual weakening of memory with age or the ravages of Alzheimer’s disease, according to the Hospital for Sick Children.