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Studies show that fatty acids are essential for memory formation

Saturated fatty acids have been demonstrated by researchers at the University of Queensland to be crucial for the brain’s ability to retain memory. Research by Dr. Isaac Akefe of the University of Queensland’s Queensland Brain Institute points to a novel treatment for neurodegenerative diseases. Moreover, he has discovered the genes responsible for memory formation. The […]

Studies show that fatty acids are essential for memory formation

Saturated fatty acids have been demonstrated by researchers at the University of Queensland to be crucial for the brain’s ability to retain memory. Research by Dr. Isaac Akefe of the University of Queensland’s Queensland Brain Institute points to a novel treatment for neurodegenerative diseases. Moreover, he has discovered the genes responsible for memory formation. The EMBO Journal published the findings. Saturated fatty acid levels have been demonstrated to rise in the brain during neuronal communication in the past, but the reason for these changes was unknown, according to Dr. Akefe.

“Now for the first time, we’ve identified alterations in the brain’s fatty acid landscape when the neurons encode a memory.
“An enzyme called Phospholipase A1 (PLA1) interacts with another protein at the synapse called STXBP1 to form saturated fatty acids.”
The brain is the body’s fattiest organ, with fatty compounds called lipids making up 60 per cent of its weight. Fatty acids are the building blocks of a class of lipids called phospholipids.

Research conducted in the lab of Professor Frederic Meunier has demonstrated that STXBP1 regulates the targeting of the PLA1 enzyme, directing communication at the brain’s synapses and coordinating the release of fatty acids. Professor Meunier stated, “Human mutations in the PLA1 and STXBP1 genes reduce free fatty acid levels and promote neurological disorders.” We employed mouse models in which the PLA1 gene was deleted to ascertain the significance of free fatty acids in the development of memory. Throughout their lives, we monitored the beginning and development of neurological and cognitive decline. We observed that their levels of saturated free fatty acid were significantly lower than those of control mice, even before their memories became impaired. This suggests that the fatty acids released by the PLA1 enzyme are important.

The research has important implications for understanding of how memories are formed.
“Our findings indicate that manipulating this memory acquisition pathway has exciting potential as a treatment for neurodegenerative diseases, such as Alzheimer’s,” Professor Meunier said.
The research team acknowledges the contributions of PhD candidates Saber Abd Elkader from the Australian Institute for Bioengineering and Nanotechnology, and Benjamin Matthews from the Queensland Brain Institute.
This is a collaborative study with the University of New South Wales, University of Strasbourg, University of Bordeaux, the Scripp Research Institute and the Baylor College of Medicine.

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