A BYU professor and researchers around the country pinned down a compound that controls how well a brain learns and forms memories.

Jeffrey Edwards, an assistant professor in the Department of Physiology and Developmental Biology, and colleagues from Brown and Duke universities, the University of Massachusetts and the McLaughlin Research Institute, discovered signal receivers in the brain are moved by a protein called myosin Vb.

This discovery opens doors for understanding how to help people learn and form stronger memories.

"People think as you age," Edwards said, "you're increasing the synapses or you're increasing the connections between neurons. But that's actually not true."

Memories are formed when connections among neurons are changed or strengthened, not from the formation of new structures.

"If you're a synapse that becomes strengthened, then the brain says, 'OK, that's an important connection. I want to keep it,'" Edwards said.

Increasing the presence or effectiveness of myosin Vb will insert more receptors at synapses, resulting in stronger connections.

Strengthening synapses will improve the function of existing cells, allowing individuals with impaired learning to handle higher levels of thinking and those with limited memory retention to improve memory formation.

Stronger synapses will not make up for memory loss resulting from dying brain cells, an outcome of diseases such as Alzheimer's, Edwards said.

However, stronger synapses may prevent neural loss from the early stages of disorders related to addiction, Alzheimer's, autism, epilepsy, schizophrenia and brain development.

Michael Ehlers, senior author of the study and a professor at the Duke University Medical Center, said, "We know that many of these diseases are disorders of synapse modification."

Before the point of losing neurons, "Early changes in Alzheimer's patients are altered synaptic plasticity," he said.

Research Details

In the brain, millions of cells send off projections that form synapses.

When cells are stimulated, Edwards said, memories form "because you've just changed a certain number of synapses."

When more receptors are available at the synapse, the change is greater and the memory is more potent.

When changes are large enough, synapses are said to reach long-term potentiation-a point when changes are sufficient to form a lasting memory. And, "the bigger your LTP, the better your memory is going to be," Edwards said.

Edwards said a goal of his research has been to find a way to ramp up LTP and improve memory and cognition.

For years, Edwards said researchers assumed receptors responsible for LTP came from a cell's primary protein-synthesizing machinery. "People tried to block this pathway and do other things and they could never block LTP. So we could never figure out where these receptors are actually coming from."

In 2004, Edwards said his team showed that one receptor, the AMPA receptor, is also formed through a recycling pathway that synthesizes broken down parts from "previously recycled AMPA receptors that were once on the membrane surface."

These studies helped lead Edwards and his team to discover the protein "motor" that moves AMPA receptors from building sites and inserts them at the synapse.

Edwards' study shows the protein motor is myosin Vb, a neural version myosin, a protein that works with actin to control movement in muscle cells.

Edwards said other researchers are already testing memory performance of rats treated with drugs that elevate myosin Vb levels.

Preliminary results show some rats that receive the drugs have sharper memories and cognition, Edwards said.

Copyright Brigham Young University 17 Nov 2008