Deleting memories with a flash of a light may be the stuff of Hollywood movies as seen in the likes of Will Smith's Men in Black but the seemingly fictional process of deleting a person's memory and restoring it back again may soon become a reality as researchers have come up with a method to erase and restore the memories of genetically engineered rats.

In the experiment described in the study "Engineering a memory with LTD and LTP" which was published in the journal Nature on June 1, researchers from the University of California San Diego created memory in rat. They also erased and restored this memory by either weakening or strengthening the connection between nerves, known as the synapses.

To create memory, the researchers stimulated nerves in the rats' brains that were genetically engineered so the rats are sensitive to light while delivering electric shock to their foot resulting in the animals to fear the stimulation.

The researchers then used low-frequency optical lasers to stimulate the same group of nerves but in a different way to erase the memories causing the rats to no longer fear the stimulation. The researchers, however, discovered, that the memory that they have erased can be restored by again stimulating the rats' nerves but using  high-frequency optical blasts causing the rats to once again exhibit fear to the stimulation.

"We can cause an animal to have fear and then not have fear and then to have fear again by stimulating the nerves at frequencies that strengthen or weaken the synapses," said study researcher Sadegh Nabavi, from the Department of Neuroscience and Section of Neurobiology at the University of California at San Diego.

If the procedure can be successfully replicated in humans, this can bring hope to patients suffering from dementia, a disease that causes those affected by it to lose their memory.

Study researcher Roberto Malinow, also from UCSD's Department of Neuroscience and Section of Neurobiology, said that the findings of the study could help patients who suffer from Alzheimer's disease, the most prevalent form of dementia.

He explained that the beta amyloid peptide in the brains of patients with Alzheimer's disease affects the synaptic connection the same way as the memory-erasing stimulation in rats suggesting that the effects of beta amyloids can be potentially reversed in Alzheimer's patients.

"Since our work shows we can reverse the processes that weaken synapses, we could potentially counteract some of the beta amyloid's effects in Alzheimer's patients," Malinow said.