Lost memories in patients suffering from Alzheimer's disease may soon be a thing of the past, thanks to a new discovery.
Long-term memories were thought to be stored within the brain's synapses, the structures which allow chemical and electrical signals to travel between neurons, or brain cells, in the organ. However, a new study shows this idea of how brains work may be inaccurate.
Damaged cells in brains can be repaired by the nervous system under favorable conditions. Researchers discovered that encouraging the nervous system to repair the cells can repair memory once lost to the condition.
"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," David Glanzman from the University of California-Los Angeles (UCLA) said.
Aplysia, a variety of marine snail, was studied to examine how the animals learned and remembered experiences. The creatures protect their gills whenever they sense danger. This withdrawal reflex was examined by the researchers, along with the motor and sensory neurons that drive the movement.
Snails in the study were given small electrical shocks in their tails, enhancing the withdrawal reflex for a few days, as well as releasing the hormone serotonin into the bloodstreams of the tiny creatures. This adaptation to behavior demonstrates long-term memory in the snails, according to researchers.
New synaptic connections formed through the release of serotonin are the underlying mechanism behind the retention of long-term memory, Glanzman and his team believe. Memories, they found, are stored when brains release proteins which form new synapses.
Concussions, injuries and other disruptions to the manufacture of these proteins prevent memories from forming, investigators stated. This explains why people do not usually remember the moments before they received a concussion.
Serotonin introduced to a Petri dish containing brain neurons caused the structures to grow new connections between motor and sensory neurons. Protein synthesis inhibitors added to the system following a dose of serotonin prevented the formation of new connections and the retention of memory, researchers found. This was not the case if the inhibitor was introduced well after the experience forming the memory.
"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," Glanzman told the press.
This knowledge could be used to develop a new generation of drugs to treat Alzheimer's disease and other ailments.
Repair of long-term memory in damaged brains and study of the role of synapses in memory storage of Aplysia was detailed in the journal eLife.
