April 25 (HealthDay News) -- A new report finds that where protein-destroying machines reside in the brain's nerve cells may help determine how memories are formed, a finding that may play a role in future treatments for Alzheimer's and other brain diseases.

Wake Forest University School of Medicine researchers studying mice discovered that cylinder-shaped proteasomes, which help control protein levels, play different roles in controlling synapse strength depending on where they are in the nerve cells of the hippocampus, an area of the brain linked to memory.

When humans or animals learn and store information in their memory, these connections between cells become stronger or weaker, Ashok Hegde, associate professor of neurolobiology and anatomy at Wake Forest, said in a prepared statement. For example, if people learn to do something better, such as playing softball, the synapses that control hand-eye coordination will become stronger. If they learn to ignore something, such as the barking of a neighbor's dog, then the synapses that control paying attention will become weaker.

The findings were published in the current issue of Learning & Memory.

It is known that the degradation of proteins, which are made by cells to control cell functions, plays an important role in memory function. The team found that proteasomes in the dendrites -- the branched parts of a neuron that conduct electrical stimulation -- limit the connection strength between cells. Proteasomes in the nucleus, which contains the cell's genetic material, help maintain synapse strength for long periods of time.

The researchers are now trying to learn how to block proteasome activity specifically in the dendrites of mice to increase the strength of synapses and of memory. In their ongoing studies, the mice will be analyzed on how well they can learn to navigate a maze.

"If we see a memory enhancement when we block the proteasome in dendrites, we can use this strategy to treat memory loss," Hegde said.

SOURCE: Wake Forest University Baptist Medical Center, news release, April 23, 2008