Cure to Alzheimer’s linked to Memory Suppressor Gene

Alzheimer’s is a terminal disease which slowly and painfully ravages the brain, degenerating neurological functions to the point where the patient is completely dependent upon caretakers. While several cures have been identified but have failed to live up to their name, the latest cure is both unorthodox and stems from an unlikely source: The Memory Suppressor Gene in the common Fruit Fly.

alzheimers new cure

Discovering the Memory Suppressor Gene

In a research study at The Scripps Research Institute led by TSRI’s Department of Neuroscience Chair Person Ron Davis, the team conducted extensive analysis of Drosophila (Fruit Fly) genes and isolated several new Memory Suppressor Genes which are responsible for:

  • Identifying important parts of memory
  • Storing the important parts of the information into brain

One gene in particular caught their attention and eliminating it resulted in enhanced memory in the flies. Doctor Davis detailed the potential of the discovery by stating that the gene functions in similar manner as most cognitive enhancers used to treat Alzheimer’s and could open doors for new treatments.

“When we knocked out this gene, the flies had a better memory — a nearly two-fold better memory,” Davis quoted. “The fact that this gene is active in the same pathway as several cognitive enhancers currently used for the treatment of Alzheimer’s disease suggests it could be a potential new therapeutic target.”

Behavior of DmSLC22A in Flies and Humans

Deactivating or over stimulating the gene (DmSLC22A) resulted in significant improvement in memory function of flies, which was characterized by:

  • 2 times improves memory identification of smells
  • Quicker response in identifying and differentiating smells

Research Associate Ze Liu explained, stating that the proteins responsible for memory functions are normally the same for fruit flies and mammals, as are the diseases.

Research Associate YunchaoGai explained the importance of DmSLC22A in developing memories. He added that drugs which deactivate this protein would prove invaluable in augmenting memory functions of patients suffering from brain related disorders.

“DmSLC22A serves as a bottleneck in memory formation. Considering the fact that plasma transporters are ideal pharmacological targets,” he continued, “drugs that inhibit this protein may provide a practical way to enhance memory in individuals with memory disorders.”

 

Future of the Research

The next step in the research as planned by Davis is to create inhibitors of this protein so Alzheimer’s patients memory functions can be improved. However, the research boasts much greater applications for many many other diseases that cause loss of memory. While such treatments may take time to be formulated and medically approved, this may prove to be an important breakthrough in treating patients with Alzheimer’s.

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