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| First Name: | Mary | | Last Name: | Michaelis | | Title: | Professor | | Advanced Degrees: | Ph.D. | | Affiliation: | University of Kansas | | Department: | Pharmacology and Toxicology | | Street Address 1: | 5064 Malott Hall | | Street Address 2: | 1251 Wescoe Hall Drive | | City: | Lawrence | | State/Province: | KS | | Zip/Postal Code: | 66045-7582 | Country/Territory: | U.S.A. | | Phone: | 785-964-3905 | | Fax: | 785-864-5219 | | Email Address: |  |
Disclosure:
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View all comments by Mary Michaelis
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Alzheimer Disease, Neurodevelopmental Disorders (Down syndrome, etc.), Tauopathies, Aging Process
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Chemistry/Pharmacology, Protein structure/chemistry, Signal transduction, Animal Models, Neurobiology, Oxidative Stress, Drug screening, Tau/Cytoskeleton
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Michaelis, M.L., Dobrowsky, R.T., and Li, G. Tau neurofibrillary pathologyl and microtubule stability. Journal of Molecular Neuroscience, 2002, 19, 289-293.
Li, G., Faibushevich, A., Sung, O.Y., Turunen, B., Georg, G., Michaelis, M.L., and Dobrowsky, R.T. Stabilization of the cyclin-dependent kinase 5 activator, p 35, by paclitaxel decreases ƒÒ-amyloid toxicity in cortical neurons. Journal of Neurochemistry, 2003, 84, 1-16.
Michaelis, M.L. Drugs targeting Alzheimer¡¦s disease: Some things old and some things new. Journal of Pharmacology and Experimental Therapeutics, 2003, 304:897-904.
Michaelis, M.L.., Ranciat, N., Chen, Y., Bechtel, M., Ragan, R., Hepperle, M., Liu, Y. and Georg, G. Protection against ƒÒ-amyloid toxicity in primary neurons by paclitaxel [Taxol„µ]. Journal of Neurochemistry, 1998, 70, 1623-1627.
Huschenbett, J., Zaidi, A., and Michaelis, M.L. Sensitivity of the synaptic membrane Na+/Ca2+ exchanger and the expressed NCX1 isoform to reactive oxygen species. Biochimica Biophysica Acta, 1998, 1374, 34-46.
Zaidi, A., Gao, J., Squier, T.C., and Michaelis, M.L. Age-related alterations in brain synaptic membrane Ca2+-ATPase in F344/BNF1 rats. Neurobiology of Aging, 1998, 19, 487-495.
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The underlying cause of the neurodegeneration. |
In vivo testing of proof-of-concept in the best mouse models of AD, i.e., those that exhibit plaques, tangles, neuronal cell loss, and cognitive deterioration! |
That loss of Ca2+ regulation and activation of an ER stress response in neurons leads to a disruption in the signaling activity mediated by the cytoskeleton and initiation of cell death cascades. Age-related alterations in the handling of Ca2+ in neurons may underlie the fact that age is the primary risk factor for AD. |
There are many steps in this cascade that still need to be tested. |
That age-dependent changes in the levels or activity of chaperones, again related to the ER, may contribute to the role of age as a risk factor and underlie the improper protein folding and aggregation that characterizes both lesions in AD brain. |
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