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Research Grants 2015

To view an abstract, select an author from the vertical list on the left.

2015 Grants - Ma

Role of eEF2 Kinase in Alzheimer’s-Associated Synaptic Failure and Memory Deficits

Tao Ma, Ph.D.
Wake Forest University
Winston-Salem, North Carolina

2015 New Investigator Research Grant

Does dysfunction of a protein called eukaryotic elongation factor 2 (eEF2) promote nerve cell damage and memory loss in Alzheimer’s disease?

The production of many different proteins is carefully regulated in the brain to maintain learning and memory processes. These proteins are often involved in maintaining the health of synapses, the tiny regions through which nerve cells send and receive chemical messages. Damage to synapses can hinder cell-to-cell communication in the brain and result in the memory loss and decline in thinking abilities associated with Alzheimer’s disease.

Research Plan
Tao Ma, Ph.D., and colleagues have recently found that a protein called eukaryotic elongation factor 2 (eEF2) is improperly regulated in the brains of people with Alzheimer’s disease, as well as in mice engineered to develop Alzheimer’s-like brain changes. Normally, eEF2 helps regulate the production of proteins vital to synaptic health. According to Dr. Ma’s hypothesis, the protein that regulates eEF2 (called eEF2 kinase, or eEF2K) becomes overactive and promotes abnormal modification of eEF2 during Alzheimer’s disease. Dysfunctional eEF2 cannot carry out its normal activities — leading to the loss of synaptic proteins that are important for maintaining cognitive abilities. For their current grant, the research team will use Alzheimer’s-like mice to examine how restoring normal eEF2 function affects brain health and memory function. They will use novel genetic and molecular techniques to restore normal eEF2 function and determine if this promotes the animals’ ability to produce synaptic proteins and improves their cognitive function.

The results of this effort could shed new light on how synapses become damaged in Alzheimer’s disease; and how such damage is related to declines in brain function. They could also lead to novel drug therapies that target the restoration of normal eEF2 function for the prevention or treatment of Alzheimer’s disease.

Alzheimer's Association International Conference | July 16-20, 2017, London, England

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