Researchers at Brandeis University have reported, in the Journal of Neuroscience, they can induce memory storage, and then biochemically erase it by manipulating a “memory molecule” protein kinase known as CaMKII.

This breakthrough could do much to benefit research into diseases of the memory, such as Alzheimer’s or dementia. It also could prove to be a breakthrough in the treatment of conditions such as epilepisy.

Just as DNA stores genetic memory, scientists have been studying the molecular basis for memory storage for years. “The core problem in memory research has been understanding what the storage molecule actually is. Identifying this molecule is essential to understanding memory itself as well as any disease of memory, ” explained lead author John Lisman. “With this study, we have confirmed CaMKII as a memory molecule.”

The research involved a process known as long-term potentiation (LTP), where neuronal synapses are stimulated electrically to strengthen them. LTP has served as a model system for studying memory, and CaMKII has been a leading candidate as a memory molecule because it can enhance synaptic transmission and is persistently activated after LTP induction. These are properties that are necessary for a memory molecule.

Just as a computer that electronically changes with the addition of new information, the molecular activity in the hippocampus, where memory is stored in the brain, changes as memory is being stored. Lisman and his colleagues in this study showed they could saturate the memory stores, and when CaMKII was chemically attacked and previous memory erased, it became possible to insert new memories in the synapses.

In conditions like epilepsy, synapses can become overly strengthened. This research shows how the synapses can be weakened by attacking memory molecules, and could be a breakthrough in development of a cure for epilepsy – as well as other conditions that are connected to memory and memory molecules.

This research complements previous work done in Lisman’s laboratory showing that when LTP is induced (as during learning), CaMKII moves into the synapse. By using fluorescent forms of CaMKII, it may be possible to determine whether the kinase leaves the synapse after an inhibitor is applied. This provides a way to directly visualize the process involved in amnesia and the forgetting process.

The research was funded by the National Institutes of Health. Further research is being planned to better understand what happens to the CaMKII after it is attacked.

From the desk of Ron White, memory speaker






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