Memory loss is one of the first signs that reveal the presence of Alzheimer’s and therefore understanding how memories are created and stored could help prevent and treat this dementia. Now, a new study by researchers at the University of Queensland (UQ), in Australia, has revealed that saturated fatty acids play a key role in consolidating memories in the brain.
Dr Isaac Akefe from UQ’s Queensland Brain Institute has uncovered the molecular mechanism and identified the genes involved in the memory creation process, opening new avenues for developing a potential treatment for neurodegenerative diseases. We previously showed “that levels of saturated fatty acids increase in the brain during neuronal communication, but we did not know what was causing these changes,” said Dr. Akefe.
“Now, for the first time, we have identified alterations in the fatty acid landscape of the brain when neurons encode a memory,” he adds, explaining that “an enzyme called phospholipase A1 (PLA1) interacts with another protein in the synapse called STXBP1 to form saturated fatty acids.
A discovery that can help treat diseases such as Alzheimer’s
The brain is the fattest organ in the body and fatty compounds called lipids make up 60% of its weight. Fatty acids are the building blocks of a class of lipids called phospholipids. The study was carried out in the laboratory of Professor Frederic Meunier and has shown that STXBP1 controls the action of the PLA1 enzyme, coordinating the release of fatty acids and directing communication in the synapses of the brain.
“Human mutations in the PLA1 and STXBP1 genes reduce free fatty acid levels and promote neurological disorders,” says Professor Meunier. And he explains that to determine how important free fatty acids were in the formation of memory, they used mouse models in which the PLA1 gene is deleted, and they “monitored the onset and progression of neurological and cognitive deterioration over time.” of their lifes”.
“We saw that even before their memories deteriorated, their levels of saturated free fatty acids were significantly lower than those of control mice.” “This indicates that this PLA1 enzyme and the fatty acids it releases play a key role in memory acquisition.”
“Manipulation of this memory acquisition pathway has great potential as a treatment for neurodegenerative diseases, such as Alzheimer’s”
The research has important implications for understanding how memories are formed. “Our findings indicate that manipulating this memory acquisition pathway has great potential as a treatment for neurodegenerative diseases, such as Alzheimer’s,” Professor Meunier said.
The study was carried out in collaboration with the University of New South Wales, the University of Strasbourg, the University of Bordeaux, the Scripp Research Institute and the Baylor College of Medicine, and its results have been published in The EMBO Journal .
