New research has revealed the process the brain uses to create crucial fatty acids and how it impacts our memory retention.
The mechanism that creates a molecule in the brain responsible for storing and acquiring memories may hold the key to treating conditions like Alzheimer's disease.
Memories are acquired and stored in the brain thanks to a specific lipid, which is a fatty acid molecule in the brain.
During earlier research on mice, scientists discovered a large amount of a lipid in their amygdala when acquiring or accessing a memory.
The amygdala is the part of the brain where memories and emotions are processed.
It was deduced that a particular lipid was responsible for acquiring memories.
Now, researchers have found the process that causes a large amount of lipids to be released when the brain is acquiring a memory.
Professor Frederic Meunier found an enzyme - called Phospholipase A - which interacts with a protein to make fatty acids in the brain during a synapse, where neurons fire electrical signals at each other to communicate information.
If there is a mutation in that enzyme or if it doesn't exist, then the fatty acid lipids aren't produced and the memories aren't acquired.
Prof Meunier from the University of Queensland said researchers taught mice how to press a lever to get a reward.
After two weeks, they recognised the system and acquired it as a memory.
"The mice that have been engineered not to have this enzyme, they just are completely and utterly unable to learn," Prof Meunier said.
Research indicated that looking at the process of creating the lipid for memory acquisition may be a key to treating neurodegenerative conditions like Alzheimer's disease.
"To treat the mechanism of neurodegeneration you need to first understand how the system works for us to acquire memories," Prof Meunier said.
"This is a big step because we have found a completely new pathway that leads to memory acquisition.
"Now we can have a look to see whether this pathway is actually sort of down-regulated in disease and aging."