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| First Name: | Craig | | Last Name: | Atwood | | Title: | Assistant Professor | | Advanced Degrees: | Ph.D. | | Affiliation: | University of Wisconsin | | Department: | Medicine | | Street Address 1: | 2500 Overlook Terrace | | City: | Madison | | State/Province: | WI | | Zip/Postal Code: | 53705 | Country/Territory: | U.S.A. | | Phone: | 608 256 1901 | | Fax: | 608 280 7291 | | Email Address: |  |
Disclosure:
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Member reports no financial or other potential conflicts of interest. [Last Modified: 1 March 2004]
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View all comments by Craig Atwood
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Aging Process, Prion Diseases, Alzheimer Disease, Stroke and Trauma
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Tau/Cytoskeleton, A-beta PP/A-beta, Molecular and Cell biology, Neurobiology, Neuropathology, Oxidative Stress, DNA microarrays, Drug screening, Stem cells, Animal Models, Apoptosis/Cell cycle, Neuroimmunology, Chemistry/Pharmacology, Protein structure/chemistry, Proteomics, Signal transduction, Epidemiology, Genetics
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University, Medical hospital
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Dr. Atwood received his Ph.D. in Biochemistry from The University of Western Australia, Perth, Australia prior to taking up a Fogarty Fellowship at the National Institutes of Health in the Laboratory of Molecular and Cellular Endocrinology, Bethesda, MD. Here, his research was directed at elucidating the molecular pathways leading to breast cancer. Following this he moved to the Genetics and Aging Unit at Massachusetts General Hospital/Harvard Medical School, Boston, first as a post-doctoral fellow and then as an Instructor of Neuroscience, where he examined basic molecular mechanisms involved in Alzheimer’s disease. In 2000 he moved to the Institute of Pathology, Case Western Reserve University as an Assistant Professor of Pathology where he began examining the relationship between the changes in reproductive hormones and aging and neurodegeneration. Dr. Atwood joined the University fo Wisconsin-Madison this past summer and has taken up the position of Research Director of the Wisconsin Alzheimer’s Institute and Research Director of the UW Memory Research program. He continues to combine his interests and expertise in reproductive endocrinology and neuroscience to understand how hormones regulate 1) neurodegeneration, and 2) aging. |
1. Atwood, C.S., Ikeda, M and Vonderhaar, B.K. (1995). Involution of mouse mammary glands in whole organ culture: a model for studying programmed cell death. Biochemical and Biophysical Research Communications 207(2), 860-867.
2. Atwood, C.S., Hovey, R., Glover, J.P., Chepko, G., Ginsburg, E., Robison, Jr., W.G. and Vonderhaar, B.K. (2000). Progesterone induces ductal side-branching of the ductal epithelium in the mammary glands of peripubertal mice. Journal of Endocrinology 167, 39-52.
3. Atwood, C.S., Huang, X., Moir, R.D., Bacarra, N.M., Romano, D., Tanzi, R.E. and Bush, A.I. (1998). Dramatic aggregation of Alzheimer Aß by Cu(II) is induced by conditions representing physiological acidosis. Journal of Biological Chemistry 273, 12817-12826.
4. Atwood, C.S., Scarpa, R.C., Huang, X., Moir, R.D., Jones, W.D., Fairlie, D.P., Tanzi, R.E. and Bush, A.I. (2000). Characterization of copper interactions with Alzheimer amyloid beta peptides: Identification of an attomolar-affinity copper binding site on amyloid beta1-42. Journal of Neurochemistry, 75, 1219-1233.
5. 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(3), 514-518.
6. Atwood, C.S., Bowen, R.L., Perry, G., Smith, M.A., (2003). Cerebrovascular Requirement for Sealant, Anti-coagulant and Remodeling Molecules that Allow for the Maintenance of Vascular Integrity and Blood Supply. Brain Research Reviews, 43, 164-178.
7. 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(10), 1217-1226.
8. 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. J. Neurochem., 88(3), 554-563.
9. 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 (epublished ahead of print).
10. 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 (in press).
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Understanding hormonal dysregulation as it relates to degenerative processes. |
McPhie DL, Coopersmith R, Hines-Peralta A, Chen Y, Ivins KJ, Manly SP, Kozlowski MR, Neve KA, Neve RL. (2003) DNA synthesis and neuronal apoptosis caused by familial Alzheimer disease mutants of the amyloid precursor protein are mediated by the p21 activated kinase PAK3. J. Neurosci. 23(17):6914-6927.
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The basic premise behind our 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. |
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