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California researchers claim they have made a breakthrough in restoring memories, the Daily Mail reports.

They say the work, in snails, could one day lead to new hope for patients in the early stages of Alzheimer's disease.

It also reveals how long term memories are stored - proving a popular theory wrong.

For decades, most neuroscientists have believed that memories are stored at the synapses — the connections between brain cells, or neurons — which are destroyed by Alzheimer's disease.

The new study provides evidence contradicting the idea that long-term memory is stored at synapses.

'Long-term memory is not stored at the synapse,' said David Glanzman, a senior author of the study, and a UCLA professor of integrative biology and physiology and of neurobiology.

'That's a radical idea, but that's where the evidence leads. The nervous system appears to be able to regenerate lost synaptic connections.

'If you can restore the synaptic connections, the memory will come back. It won't be easy, but I believe it's possible.'

The findings were published recently in eLife, a highly regarded open-access online science journal.

Glanzman said the research could have significant implications for people with Alzheimer's disease.

Specifically, just because the disease is known to destroy synapses in the brain doesn't mean that memories are destroyed.

'As long as the neurons are still alive, the memory will still be there, which means you may be able to recover some of the lost memories in the early stages of Alzheimer's,' he said.

Glanzman added that in the later stages of the disease, neurons die, which likely means that the memories cannot be recovered.

Glanzman's research team studies a type of marine snail called Aplysia to understand the animal's learning and memory.

The Aplysia displays a defensive response to protect its gill from potential harm, and the researchers are especially interested in its withdrawal reflex and the sensory and motor neurons that produce it.

They enhanced the snail's withdrawal reflex by giving it several mild electrical shocks on its tail.

The enhancement lasts for days after a series of electrical shocks, which indicates the snail's long-term memory.

Glanzman explained that the shock causes the hormone serotonin to be released in the snail's central nervous system.

After erasing the memory, scientists repeated the experiment in the snail, and then gave the animal a modest number of tail shocks — which do not produce long-term memory in a naive snail — the memory they thought had been completely erased returned.

This implies that synaptic connections that were lost were apparently restored.

'That suggests that the memory is not in the synapses but somewhere else,' Glanzman said.

'We think it's in the nucleus of the neurons. We haven't proved that, though.'

The researchers also wanted to understand whether synapses disappeared when memories did.

To find out, they counted the number of synapses in the dish and then, 24 hours later, added a protein synthesis inhibitor. One day later, they re-counted the synapses.

What they found was that new synapses had grown and the synaptic connections between the neurons had been strengthened; late treatment with the protein synthesis inhibitor did not disrupt the long-term memory.

Long-term memory is a function of the growth of new synaptic connections caused by the serotonin, said Glanzman, a member of UCLA's Brain Research Institute.

As long-term memories are formed, the brain creates new proteins that are involved in making new synapses. If that process is disrupted — for example by a concussion or other injury — the proteins may not be synthesized and long-term memories cannot form.

This is why people cannot remember what happened moments before a concussion.

'If you train an animal on a task, inhibit its ability to produce proteins immediately after training, and then test it 24 hours later, the animal doesn't remember the training,' Glanzman said.

'However, if you train an animal, wait 24 hours, and then inject a protein synthesis inhibitor in its brain, the animal shows perfectly good memory 24 hours later.

'In other words, once memories are formed, if you temporarily disrupt protein synthesis, it doesn't affect long-term memory.

'That's true in the Aplysia and in human's brains.'