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| Edmond Teng, M.D., Ph.D. Visiting Assistant Professor of Neurology Dept of Neurology University of California, Los Angeles
Dr. Edmond Teng's Beeson research examines levels of AD-related proteins in the cerebrospinal fluid of a model of AD in genetically-modified rats. These animals develop AD-related changes over a shorter periods of observation and appear to improve with experimental treatments administered in the laboratory. Therefore, they provide an excellent opportunity to determine whether measurements of proteins in the cerebrospinal fluid are useful for measuring early responses to effective therapeutics. The results of Dr. Teng's research may help in the design of future clinical trials of treatments for AD, to make them smaller, faster, and more cost-effective so that a greater number of potential therapeutic agents can be evaluated in a shorter period of time, and the most promising drugs can be identified at an earlier stage in the development process. Dr. Teng received his MD and his PhD in Neurosciences from the University of California, San Diego. He completed an internship in Medicine, a residency in Neurology, and a fellowship in Dementia and Behavioral Neuroscience Research at the University of California, Los Angeles, and a Special Fellowship in Geriatric Neurology at the VA Greater Los Angeles Healthcare System.
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| Primary Research (for Beeson Program): Assessment of Biomarkers and Behavior in a Transgenic Rat Model of Alzheimer's Disease
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There are currently a multitude of clinical trials that are evaluating potential new treatments for Alzheimer's disease (AD). The primary methods for evaluating new therapies are focused on changes in memory function, behavioral symptoms, and level of everyday functioning. Unfortunately, researchers' abilities to measure such changes are relatively insensitive to early or small improvements, which results in clinical trials that are longer in duration, require more subjects, and cost more money to complete. An alternative strategy is to look for early changes in biological markers of the disease, such as the levels of AD-related proteins in the cerebrospinal fluid. However, due to the current dearth of effective, disease-modifying treatments for AD, it has been difficult to evaluate these methods in human subjects.