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John Kauwe, Ph. D.

Brigham Young University Professor

I was trained in the molecular genetics of Alzheimer’s disease, collection and analysis of cerebrospinal fluid biomarker data, and analysis of genome-wide association data while completing my PhD with Dr. Alison Goate at the Washington Univeristy School of Medicine. During my PhD I also worked closely with Drs. Alan Templeton, James Cheverud, and Brian Suarez, developing a broad skillset in population and statistical genetics. As a postdoctoral fellow I continued my work on Alzheimer’s disease while obtaining additional training from Dr. John Rice in statistical genetics and Dr. David Holtzman in neuroscience. I have been involved extensively in the NIH funded Alzheimer’s Disease Genetics Consortium (ADGC). I participated in the original planning meeting in 2007 and Dr. Goate and I wrote one of the aims of the successfully funded U01 proposal. I have continued my involvement in the ADGC and I am the PI of several special analysis groups within the consortium. In addition, Dr. Gerard Schellenberg (PI of the ADGC) is the mentor for my Mentored New Investigator Grant from the Alzheimer’s Association. Dr. Schellenberg has committed considerable effort over the next three years to serve as my early career mentor.

In the short time since I began my graduate studies at Washington University in St. Louis I have been very productive, publishing 35 manuscripts (including eleven as the first or last author) in the genetics of complex traits. The focus of my research has been on using quantitative endophenotypes to understand the genetics of Alzheimer’s disease. Through a series of manuscripts I have demonstrated the utility of genetic studies of endophenotypes both in identifying novel disease modifying variants and in understanding biological mechanisms by which known risk genes exert their effects. Manuscripts 5, 9 and 13 in section C are examples of how I have implemented this approach to find novel variants that cause AD or influence the onset or progression of disease. Manuscripts 10 and 12 in section C demonstrate how this approach can inform about the biological mechanisms by which risk variants act. I have continued to pursue this approach and I will soon submit manuscripts outlining the results of genome-wide association studies for CSF Aβ42 and tau levels. In addition, my CV demonstrates I am an effective and efficient collaborator and have published papers with many different investigators on a variety of AD-related topics.