California Researchers May Have Made A Breakthrough In Restoring Lost Memories Due To Alzheimer Disease


There’s a new research study that claims lost memories can be restored for those suffering from Alzheimer disease. This is according to a California based researched group basing their findings on their experiments involving snails. This is a pioneering effort, the first to debunk decades of belief that once memories are lost due to the disease, there’s no way they can be restored.


Most neuroscientists are of the agreement that the brain synapses are responsible for maintaining long term memories and that once they are damaged by Alzheimer’s disease, the memories are lost with them. These synapses act as bridges between brain cells, known as neurons.


“Long-term memory is not stored at the synapse,” said David Glanzman. He is the senior author of the research study, 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.”

“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 continued.

You can read the results of the research published in elife, an open access online publication which gets coverage from nationally recognized and highly trusted media publications such as The New York Times and National Geographic.

The research could have a profound effect on people who are suffering from Alzheimer Disease, according to Glanzman.

The Aplysia snail is the subject matter of Glanzman’s research team, aiming to comprehend its learning ability and memory pattern.

The animal is known for its ability to protect its gill from any external threats. The research team wanted to explore how the withdrawal reflex works and the involvement of sensory and motor neurons that made it possible.

By consistently applying mild electrical shocks on its tail, they were able to increase the animal’s withdrawal reflex. The process was carried out for several days, affecting the snail’s long term memory.

The shock served to act as catalyst in releasing serotonin hormones in the central nervous system, Glanzman explained. The scientists removed the snail’s memory then they applied the mild electrical shocks on its tail, and the memory they expected to have been completely eradicated apparently came back. This means that the cut synaptic connections had been 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. 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.”

Another area of deep interest to the scientists is to find out whether there is a relationship between lost memories and disappearing synapses. What they did was to they put a specific number of number of synapsis in a petri dish. After 24 hours had elapsed they added a protein synthesis inhibitor.

Another 24 hours later they took s record of the number of the synapse in the dish and they discovered that there were not only new neuron formation but also there was a marked improvement in the synaptic connections between the neurons.

This is the reason why individuals find it hard to recall what occurred right after the 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.”



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