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| John Hardy, Ph.D., Senior Investigator |
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Dr. Hardy received his B.S. degree in 1976 from Leeds University, England. He received his Ph.D. degree in 1979 from Imperial College, London, where he worked on dopamine neurotransmission. After postdoctoral work in Newcastle upon Tyne in England and at the Swedish Brain Bank in Umea, working on the neurochemistry of Alzheimer's disease, Dr. Hardy returned to Imperial College in 1983 as an Assistant Professor where he investigated the genetics of Alzheimer's disease. He was promoted to Associate Professor in 1989, and then in 1992 moved to a chair at the University of South Florida, Tampa. In 1996, Dr. Hardy moved to the Mayo Clinic, where he became Chair of Neuroscience in 1999. In 2001 he moved to the NIA as Chief of the Laboratory of Neurogenetics. Dr. Hardy is a recipient of the Potamkin, MetLife and Allied Signal Awards for his work on Alzheimer's disease. His laboratory studies the genetics and molecular pathogenisis of neurological disease.
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Staff:
- Melisa Baptista, Ph.D., Staff Scientist baptista@mail.nih.gov
- Digamber Borgaonkar, Ph.D., Volunteer borgaonk@mail.nih.gov
- Jaime Duckworth, M.Sc, Investigator jaimed@mail.nih.gov
- Miss. Crystal Evey, B.S., Student eveyc@mail.nih.gov
- J. Raphael Gibbs, B.S., Special Expert gibbsr@mail.nih.gov
- Melissa Hanson, B.S., Patient Coordinator hansonm@mail.nih.gov
- Deirdra Turman, Administrative Assistant turman@mail.nih.gov
Research Interests:
Since 1986, our lab has had a very simple philosophy: find the genes and mutations which cause neurological disease: take those genes and mutations into cells and into transgenic animals and make animal (transgenic mouse) models of them to better understand the disease processes and to use those models to test therapies. This simple philosophy underpins the current organization of the lab. However, for many diseases we have been interested in, particularly Alzheimer?s disease, all the genes involved in the simple forms of the disease have been identified (the amyloid gene and presenilin 1 and 2). For Parkinson?s disease some of the ?simple? genes have been identified (synuclein and parkin) but others remain, and for frontal temporal dementia, the tau gene has been identified but there are likely to be others. Increasingly for these diseases, and also for other diseases we are interested in, such as stroke, we will be searching for risk factor genes such as the apolipoprotein E gene in late onset Alzheimer?s disease. A major focus of work in the lab will be to develop and use strategies designed to find such risk factor genes.
Finally, we will be continuing to use this genetic information to help us build animal models of disease which will be useful, both for developing an understanding of the pathogeneses of the disease, and also for developing treatments for these devastating disorders.
In Alzheimer?s disease, our work and that of others, suggested that mutations which led to disease signposted a pathologic biochemical pathway which lead to disease pathogenesis. In AD this pathway seems to be the ?amyloid cascade?. We think it is likely that this type of relationship exists between the different gene products in other diseases and this belief informs the cell biology work we undertake. Thus, we will be continuing to work on Alzheimer?s disease cell biology, both the presenilins and APP, and with other pathogenic gene products as we and others identify them. This philosophy will also underpin our work on the cell biology of Parkinson?s disease and the other diseases we are interested in.
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Selected Recent Publications:
Lewis J, Dickson DW, Lin WL, Chisholm L, Corral A, Jones G, Yen SH, Sahara N, Skipper L, Yager D, Eckman C, Hardy J, Hutton M, McGowan E (2001) Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP, Science 2001 Aug 24;293(5534):1487-91.
All Selected Publications
Contact Information:
Dr. John Hardy
Laboratory of Neurogenetics, NIA
Porter Neuroscience Research Center
Building 35, Room 1A-1014
35 Convent Drive , MSC 3707
Bethesda, MD 20892-3707
Telephone: (301) 451-3829 (office),
(904) 953-7356 (laboratory),
(904) 953-7370 (fax)
Email: hardyj@mail.nih.gov
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