Alzheimer's is characterised by profound memory loss and synaptic failure. Although the exact cause of Alzheimer's remains unclear, it is well established that maintaining memory and synaptic plasticity requires protein synthesis.
"All completed clinical trials of new drugs have failed so there is clearly a need for novel therapeutic targets for potential treatments," said Ma.
The team have shown AD-associated activation of a signalling molecule termed eEF2K leads to inhibition of protein synthesis.
In the study published in the Journal of Clinical Investigation, they wanted to determine if suppression of eEF2K could improve protein synthesis capacity and consequently alleviate the cognitive and synaptic impairments associated with the disease.
The researchers used a genetic approach to repress the activity of eEF2K in two different Alzheimer's mouse models.
They found that genetic suppression of eEF2K prevented memory loss in those animal models and significantly improved synaptic function.
"These findings are encouraging and provide a new pathway for further research," Ma said.
The team hopes to test this approach in additional animal studies and eventually in human trials using small molecule inhibitors targeting eEF2K.
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