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John Kauwe, Ph. D.

Brigham Young University Professor

Dr. Kauwe 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 his PhD with Dr. Alison Goate at the Washington Univeristy School of Medicine. During his PhD he 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 he continued his work on Alzheimer’s disease while obtaining additional training from Dr. John Rice in statistical genetics and Dr. David Holtzman in neuroscience. Dr. Kauwe has been involved extensively in the NIH funded Alzheimer’s Disease Genetics Consortium (ADGC). He participated in the original planning meeting in 2007 and Dr. Goate and wrote one of the aims of the successfully funded U01 proposal. He continued his involvement in the ADGC and is the PI of several special analysis groups within the consortium. In addition, Dr. Gerard Schellenberg (PI of the ADGC) is the mentor for his Mentored New Investigator Grant from the Alzheimer’s Association. Dr. Schellenberg has committed considerable effort over the next three years to serve as his early career mentor.

In the short time since Dr. Kauwe began his graduate studies at Washington University in St. Louis he has been very productive, publishing 35 manuscripts (including eleven as the first or last author) in the genetics of complex traits. The focus of his research has been on using quantitative endophenotypes to understand the genetics of Alzheimer’s disease. Through a series of manuscripts he has 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 Dr. Kauwe has 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. He has continued to pursue this approach and will soon submit manuscripts outlining the results of genome-wide association studies for CSF Aβ42 and tau levels. In addition, his CV demonstrates an effective and efficient collaborator who has published papers with many different investigators on a variety of AD-related topics.