Aside from being deadly, the other major devastating effect of Alzheimer’s Disease is the progressive loss of memory and identity. Alzheimer’s is a degenerative neurological disease affecting over five million Americans that presents as a loss of neuronal synapses, or connections, in the brain. Progress in understanding and potentially preventing or treating Alzheimer’s has been slow despite tremendous scientific efforts. However, a new study by neuroscientists at the UCLA Brain Research Institute may offer some promise.

The accepted explanation for how long-term memory is stored in the brain is that they are maintained in the synapses — the tiny connections between nerve cells — which tend to disappear over time in Alzheimer’s patients. Research by David Glanzman and colleagues challenges this long-held notion of how memories are stored.

“Long-term memory is not stored at the synapse,” said Glanzman, senior author of the study and UCLA professor of integrative biology and physiology and of neurobiology, in a statement. “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 study was conducted in a species of sea snail called Aplysia, a research model organism popular among neuroscientists and behavior scientists. More specifically, the scientists were keenly interested in the animal’s withdrawal reflex, a sensory- and motor neuron-mediated reaction to potential harm of the snail’s gills.

The research team was able to enhance the snail’s withdrawal reflex by giving it a series of mild electrical shocks on its tail. The observed reflex enhancement persists for days, indicating that the snail’s long-term memory had become involved. The shocks caused the neurotransmitter serotonin to be released in the snail’s central nervous system. The serotonin went on to evoke the formation of new synapses.

The researchers found that by interrupting the formation of new synapses, they could essentially prevent the reflex enhancement. On the other hand, if they interfered with the production of new proteins after the synapses were already formed, then the enhancement remained in place.

“Once memories are formed, if you temporarily disrupt protein synthesis, it doesn’t affect long-term memory,” said Glanzman. “That’s true in the Aplysia and in human’s brains.”

Interestingly, the memories could be erased by hitting the neurons once with serotonin and preventing synapses from forming by blocking the synthesis of new proteins. Then the memories were restored with a new series of electrical shocks. The research sheds new light on long-term memory by shifting attention for where it is stored away from the synapses more centrally toward the nerve cell bodies.