Department of Medicine
University of Wisconsin
CRAIG S ATWOOD
Contact Information
2500 OVERLOOK TERRACE
MADISON, WI 53705
Biography
| Education | ||
|---|---|---|
| 1984 | B. Sc (Hon.) in Biochemistry | The University of Western Australia, Perth, Western Australia |
| 1993 | PhD (Biochemistry) | The University of Western Australia, Perth, Western Australia |
| 1993-1995 | Fogarty Fellow | Laboratory of Molecular and Cellular Endocrinology National Cancer Institute, National Institutes of Health Bethesda, MD |
| 1995-1996 | Research Fellow in Neurology | Harvard Medical School, Boston, MA |
Current Appointments:
2003 - present
Assistant Professor, Dept. of Medicine (Section of Geriatrics & Gerontology), UW-Madison
Research Director, Wisconsin Alzheimer's Institute, Madison
Research Director, UW Memory Research Program, UW-Madison
Adjunct Assistant Professor of Pathology, Case Western Reserve University, Cleveland, OH
Adjunct Senior Lecturer, Edith Cowan University, School of Biomedical & Sports Science, Faculty of Computing, Health and Science, Perth, Western Australia
Dr. Craig Atwood is an Assistant Professor of Medicine at the University of Wisconsin and an investigator with the Geriatric Research, Education and Clinical Center at the William S. Middleton memorial Veterans Administration Hospital in Madison. Dr. Atwood and a colleague (Dr. Bowen) have proposed a novel theory of aging based on the modulation of cell cycle signaling by reproductive hormones. The basic premise behind the research is that hormones that regulate reproduction in mammals act in an antagonistic pleiotrophic manner to control aging via cell cycle signaling; promoting growth and development early in life in order to achieve reproduction, but later in life, in a futile attempt to maintain reproduction, become dysregulated and drive senescence. In essence, this theory proposes that reproductive hormones regulate our aging by modulating the life cycle of cells. With regard to this theory, Dr. Atwood's laboratory examines two major research themes. The first is to examine the role of the hypothalamic-pituitary gonadal axis in neurodegeneration associated with Alzheimer's disease (i.e. in synaptic and neuronal loss, amyloid deposition and neurofibrillary tangle formation). Current research projects in this area include investigation of the hormonal regulation of neuronal: 1). gene/protein expression with aging and in particular following menopause/andropause, 2). APP processing and amyloid deposition, 3). cell proliferation and re-entry of differentiated neurons into the cell cycle, 4). oxidative stress and 5). metal ion homeostases. The second research theme examines the modulation of healthy aging and lifespan. Current research projects include understanding the role of pituitary hormones in modulating healthy aging and lifespan, with an emphasis on gene expression and utilizing pituitary hormone lowering drugs to dissect hormonal pathways that promote longevity and their mechanism of action. A number of different animal (from C. elegans to humans) and in vitro (cell lines and primary cells) models are used to address how the dysregulation of the hypothalamic-pituitary-gonadal axis during menopause/ andropause drives both aging and age-related diseases, particularly Alzheimer's disease. Recent experimental work has been instrumental in showing that leuprolide acetate, currently used for the treatment of prostate cancer, may be effective in reversing Alzheimer's disease pathology.
Search for Craig Atwood's literature abstracts on PubMed
Bowen, R.L. and Atwood, C.S. (2004). Living and Dying for Sex: A theory of aging based on the modulation of cell cycle signaling by reproductive hormones. Gerontology 50, 265-290.
Bowen, R.L., Verdile, G., Liu, T., Perry, G., Smith, M.A., Martins, R.N. and Atwood, C.S. (2004). Luteinizing hormone, a reproductive regulator that modulates the processing of amyloid-ß protein precursor and amyloid-ß deposition. Journal of Biological Chemistry 279, 20539-45.
Liu, T., Perry, G., Chan, H.W., Verdile, G., Martins, R.N., Smith, M.A. and Atwood, C.S. (2004) Amyloid-ß-induced toxicity of primary neurons is dependent upon differentiation associated increases in tau and cyclin-dependent kinase 5. Journal of Neurochemistry, 88, 554-563.
Atwood, C.S., Barzilai, N., Bowen, R.L., Brown-Borg, H.M., Jarrard, D.F., Fu, V.X., Heilbronn, L.K., Ingram, D.K., Ravussin, E., Schwartz, R.S., Weindruch, R. (2003). Pennington Scientific Symposium on Mechanisms and Retardation of Aging. Experimental Gerontology 38, 1217-1226.
Bowen, R.L., Smith, M.A., Harris, P.L.R., Kubat, Z., Martins RN, Castellani, R.J., Perry, G. and Atwood, C.S. (2002). Elevated luteinizing hormone expression colocalizes with neurofibrillary tangles in Alzheimer disease. Journal of Neuroscience Research, 70, 514-518.
Dr. Atwood is the author of more than 45 peer-reviewed research reports and 50 review articles. He serves on the editorial board of the Journal of Alzheimer's Disease and Current Alzheimer's Research, reviews articles for numerous journals and serves on a number of grant and advisory boards.