A new key to the treatment of Alzheimer's disease: memory suppression gene

Release date: 2016-04-28

Scientists from the Scripps Research Institute, one of the top ten US life science research institutes, have recently discovered dozens of memory-suppressing genes. The discovery of these genes provides a new way to develop new treatments for cognitive disorders represented by Alzheimer's disease.

The research team led by Ron Davis, head of the Brain Science Department at Scripps Florida, published their latest research on the April issue of the Cell publication Neuron on April 14. By screening 3,500 genes that are highly expressed in the brain, they discovered more than 40 genes that selectively store key information during learning and memory. One of the genes, DmSLC22A, aroused their interest.

“When we knocked down the gene, the memory of the animal nearly doubled!” Davis said. “We found that this gene is in parallel with the FDA-approved gene for the treatment of Alzheimer's disease. We may have found a solution to the current poor drug efficacy."

"Memory-related genes are highly conserved in mammals and fruit flies," said Liu Ze, a co-first author of the article. "Most human brain disease-related genes can find homologous factors in Drosophila."

This gene belongs to the transmembrane transporter family and is responsible for the selective transport of organic molecules into cells. In the case of DmSLC22A, it is responsible for transporting neurotransmitters in the nervous processes to downstream neurons. The specific function of this gene is responsible for removing acetylcholine from the neuronal processes of the mushroom body and terminating neurotransmission. When the gene is inhibited, a stronger and longer-lasting signal is accumulated in the neurite to enhance the memory of the organism. "The DmSLC22A is the bottleneck in the process of biological learning and memory formation. The DmSLC22A inhibitor will be a good improvement considering that the transmembrane transporter family protein is recognized as the ideal drug target site," said the author. Memory of drugs."

"Next, we will establish an effective fluorescence screening method to find inhibitors of this gene, providing accurate and effective drugs for the treatment of memory decline in neurodegenerative diseases," Dr. Davis added.

Source: Biopass

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