This new mechanism could prevent Alzheimer's disease!



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These results are encouraging and offer a new avenue of research to identify prevention mechanisms of Alzheimer's disease.

This new mechanism could prevent Alzheimer's disease

Alzheimer's disease is characterized by profound memory loss

The researchers have identified a new mechanism and a potential new therapeutic target for Alzheimer's disease (AD), says a new study on the mouse.

Alzheimer's disease is characterized by profound memory loss and synaptic failure. Although the exact cause of the disease remains unclear, it is well established that maintaining memory and synaptic plasticity requires protein synthesis.

The function of the synapse is to transfer the electrical activity (information) from one cell to another.

"Alzheimer's disease is such a devastating disease that there is currently no treatment or effective treatment," said Tao Ma, badistant professor at the Wake Forest School of Medicine in the United States.

"All completed clinical trials of new drugs have failed, so it is clearly necessary to define new therapeutic targets for potential treatments."

For the study, the team showed that AD-related activation of a signaling molecule called eEF2K induces inhibition of protein synthesis.

In addition, they wanted to determine whether the suppression of eEF2K could improve the protein synthesis capacity, thereby attenuating the cognitive and synaptic alterations badociated with the disease.

They used a genetic approach to suppress the activity of eEF2K in murine models of Alzheimer's.

The results, published in the Journal of Clinical Investigation, showed that genetic suppression of eEF2K prevented memory loss in these animal models and significantly improved synaptic function.

"These results are encouraging and offer a new avenue for further research," Ma said.

The team then plans to test this approach in additional animal studies and, possibly, human trials using small molecule inhibitors targeting eEF2K.

(This story has not been changed by NDTV staff and is generated automatically from a syndicated feed.)

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