Washington, April 24 : A study on mice led by an Indian-origin researcher at Wake Forest University School of Medicine suggests that cylinder-shaped protein-destroying machines in nerve cells, called proteasomes, may play an important role in memory formation.
Dr. Ashok Hegde, associate professor of neurolobiology and anatomy, says that his findings may have important implications for treating Alzheimer's and other brain diseases.
"We hope to exploit this finding to manipulate memory and find ways to make it better. Our goal is to develop a new strategy for treating memory loss," said Hegde, whose study appears in the journal Learning and Memory.
He revealed that the new findings spring from the study of nerve cells in the hippocampus, a region of the brain associated with memory coding and storing of memory.
He employed in his study the information that the synapses (connections between nerve cells) play an important role in memory.
"When humans or animals learn and store what is learned in their memory, these connections between cells become stronger or weaker. For example, if we learn to do something better, such as playing softball, the synapses that control our hand-eye coordination will become stronger. If we learn to ignore something, such as the barking of a neighbour's dog, then the synapses that control paying attention will become weaker," said Hegde.
Hegde and his colleagues studied in mice how protein degradation affects connection strength because they already knew that the degradation of proteins, which are made by cells to control cell functions, plays an important role in memory function.
They found that the proteasomes in different parts of nerve cells plays different roles in controlling synapse strength, and presumably in memory.
Hegde's made that this discovery by studying connection strength with and without a chemical that blocks activity of the proteasomes.
The researchers observed that proteasomes located in the dendrites, the branched projections of a neuron that act to conduct the electrical stimulation, limit the strength of the connections between cells.
Proteasomes in the nucleus, the part of the cell that contains genetic material, help maintain synapse strength for long periods of time.
Hegde is now planning a study to learn how to block proteasome activity, specifically in the dendrites, to increase the strength of synapses and memory. His team is presently conducting studies in mice to block proteasome activity in the dendrites, using mazes to test memory.
"If we see a memory enhancement when we block the proteasome in dendrites, we can use this strategy to treat memory loss," said Hegde.
He further said that the results of the study were significant, for they might lead to the development of potential therapies to treat human diseases that affect memory.
"Protein degradation is abnormal in many brain diseases, including Alzheimer's. Having a thorough knowledge of how protein degradation works to changes synapses is a first step to finding a cure for memory loss," said Hegde.