Scripps Research Institute Logo Eating the right food greatly helps to enhance an individual’s memory capacity, therefore selecting necessary food stuffs becomes essential. Now, experts from the Florida campus of The Scripps Research Institute reveal an approach which plays a vital role in the development of long-term memory.

The findings ponder on how memory is generally formed, thereby paving a path to come up with novel treatments for memory disorders. Scientists identified that main stimulator of memory formation is myosin II. This element is a motor protein significant to cell movement and growth.

“By showing for the first time that myosin II acts as the principal organizer of memory formation, we are that much closer to identifying the signaling pathways that activate this motor protein in the brain,” commented Gavin Rumbaugh, an assistant professor in the Department of Neuroscience at Scripps Florida who led the study. “Once we’re able to do that, we can begin to develop potential treatments that could restore memory in people who suffer from cognitive disorders like Alzheimer’s disease.”

Experts highlighted that myosin II derives a mechanical process that is part of the complex process of memory formation. Myosin II merges the beginning of long-term potentiation.

“Stimulation in the brain turns on these myosin motors and this triggers the growth of F-actin that ultimately solidifies the enhancement of neuronal communication. Growth and strengthening of synapses is a process that the brain uses to record our experiences. We are just now beginning to understand the physical substrates within synapses that enable the storage of our life experiences,” Rumbaugh added.

This is a process that improves signal transmission between two neurons in the creation of memory, stabilization of synaptic plasticity and restructuring of neurons’ F-actin which is a cellular polymer that enhances growth of synapses.

“Many parallel brain processes have to be activated to store information. If any one of them is disrupted, the information doesn’t get stabilized and the memory is lost. Myosin II is a central regulator of this process and if you could pharmacologically control myosin II, you could potentially regulate memories at will,” Rumbaugh further added.

The role of F-actin described in the analysis is consistent with the long-standing idea that long-term potentiation is dependent on modifications to the synaptic architecture. This highlights that the dynamic restructuring stimulated by myosin II represents an early step in information encoding.

These findings were published in the journal Neuron on August 26, 2010.