Second pathway to brain’s memory function uncovered

By Dr. Ananya Mandal, MDOct 4 2010

Australian and US scientists have successfully identified a new mechanism by which the brain learns and stores memories. This could spell hope for brain injuries and diseases like Alzheimer’s disease.

Lead researcher Bryce Vissel of Sydney's Garvan Institute said that this finding may challenge the current knowledge of the brain’s methods to capture and encode information. “In terms of understanding learning and memory mechanisms in the brain, it's quite a fundamental shift in our understandings…And I think it's got the potential to ultimately influence not only our understanding of brain function, but also drug development and our psychological approaches to treating people with Alzheimer's,” he said.

The study spanned over six years and utilized mice to show the impact on the brain function when a particular receptor -- previously deemed critical to learning something for the first time -- was chemically switched off. NMDA receptor in the hippocampus (a region of the brain) explained Vissel was considered to be “important not only for forming new memories, but was thought to be essential for all memory formation.” The results showed that while the brain uses the receptors when learning an experience for the first time, but that these were not essential for handling the subsequent learning of a similar event because another molecular mechanism was used. This secondary pathway, hopes the team, can be replicated, either using medication or other therapies, to treat patients with brain injuries or diseases such as Alzheimer's or Parkinson's.

Vissel said, “The exact implications of this research is that there is a separate mechanism of learning in the brain, it seems to be employed on what we call second learning… It's like a new lens on your camera, you've just got a new way of looking at learning and memory. You think, 'Oh, you can exploit this in so many ways'”

The findings appeared in the Tuesday online issue of the journal PLoS ONE.