The Alzheimer’s Association announced this year’s research awards. Locally, we were thrilled to learn of the $240,000 award to local Baylor researcher Hui Zheng PhD. In 2003 Dr. Zheng was the recipient of an Alzheimer’s Association Zenith fellowship. We met with Dr. Zheng to learn of her new research. To view the full list of 2006 research award winners please click on this link.

What is the focus of your research?

Our lab is studying the communication between neurons. This cross-talk requires AcetylCholine (ACH). There is a loss of ACH in Alzheimer’s disease. We’re interested in the pathway and the process of ACH production and reabsorption. Specifically, we’re continuing to study the role of plaque-forming Amyloid Precursor Protein (APP) in the pathway of ACH. The Zenith Award funded our research which confirmed the role of APP in learning and memory within the central nervous system. We published the first paper describing the role of APP in vivo in the Journal of Neuroscience in 2005. We will continue with this research by defining the specific role of APP within the ACH pathway.

What is the design for this study?

Our research will study the function of APP in two ways. During the Zenith project, we developed genetically altered mice which lack APP in their cholinergic neurons. Using these mice, we will learn about the role of APP by studying the ability of neurons to communicate while manipulating externally added APP. That communication will be measured by recording the changes in electrical current passing between neurons.

We will also study the role of APP in the ACH pathway. We will label choline with a radio-isotope marker, then track its recycling by the neuron as we manipulate the presence of APP.

Through the combination of in vivo and in vitro studies during this project, we believe we will gain significant insight into the role of APP in the loss of ACH observed in Alzheimer’s disease.

Would your research have clinical application for AD treatment?

The current AD therapies try to correct the deficiency of ACH by blocking its breakdown. The problem with these therapies is the long-term neuron fatigue resulting in loss of drug effectiveness. Our greater understanding of the ACH pathway may facilitate development of drug therapies that would be more effective for a longer period of time.