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| First Name: | Robert | | Last Name: | Bowser | | Title: | Associate Professof | | Advanced Degrees: | Ph.D. | | Affiliation: | University of Pittsburgh Sch Medicine | | Department: | Pathology | | Street Address 1: | BST S-420 | | Street Address 2: | 3500 Terrace St. | | City: | Pittsburgh | | State/Province: | PA | | Zip/Postal Code: | 15261 | Country/Territory: | U.S.A. | | Phone: | 412-383-7819 | | Email Address: |  |
Disclosure:
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Member reports no financial or other potential conflicts of interest. [Last Modified: 16 October 2003]
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View all comments by Robert Bowser
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Alzheimer Disease, Aging Process, Neuromuscular Disorders (ALS, etc.)
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A-beta PP/A-beta, Molecular and Cell biology, Neuropathology, Proteomics, Animal Models, Apoptosis/Cell cycle, Oxidative Stress, Signal transduction
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Dr. Bowser's research interests are in determining the molecular and cellular basis of neurodegeneration in human diseases. While many neurologic diseases exhibit loss of specific neuronal subtypes, little is known about the mechanisms that regulate neuronal cell death. Recent studies in the laboratory have focused upon a group of interacting transcription factors and the role they play in neurodegeneration in Alzheimer's disease and amyotrophic lateral sclerosis (ALS). We hypothesize that altered function of nuclear proteins regulates gene expression that ultimately dictates the survival or death of the neuron during human disease. Another focus of the lab is to identify biomarkers in the cerebral spinal fluid that can specifically diagnose ALS. These biomarkers will also be used to test drug efficacy in clinical trials of drugs to impede progression of this disease. |
Ranganathan, S., and Bowser, R. (2003). Alterations in G1 to S phase cell cycle regulators during amyotrophic lateral sclerosis. Am. J. Pathol., 162: 823-835.
Jordan-Sciutto, K.L., Malaiyandi, L.M., and Bowser, R. (2002). Altered distribution of cell cycle transcriptional regulators during Alzheimer’s Disease. J. Neuropathol. Exp. Neurol., 61: 358-367.
Walker, M.P., Schlaberg, R., Hays, A.P., Bowser, R., and Lipkin, W.I. (2001). Absence of echovirus sequences in brain and spinal cord of ALS patients. Ann. Neurol., 49: 249-253.
Jordan-Sciutto, K.L., Dragich, J.M., Caltagarone, J.M., Hall, D.J., and Bowser, R. (2000). Fetal Alz-50 clone 1 (FAC1) protein interacts with the myc associated zinc finger protein (ZF87/MAZ) and alters its transcriptional activity. Biochemistry, 39: 3206-3215.
Jordan-Sciutto, K.L., Dragich, J.M., Rhodes, J.L., and Bowser, R. (1999). Fetal Alz-50 clone 1, a novel zinc-finger protein, binds a specific DNA sequence and acts as a transcriptional regulator. J. Biol. Chem., 274: 35262-35268.
Beites, C.L., Xie, H., Bowser, R., and Trimble, W.S. (1999). The septin CDCrel-1 binds syntaxin and inhibits exocytosis. Nature Neuroscience, 2: 434-439.
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Our lack of knowledge concerning the initiating factors that lead to the development of Alzheimer disease related neuronal cell death. This knowledge void also includes the multiplicity of ways (including aging) that leads one to a clinical diagnosis of AD. |
Longitutinal proteomics and imaging studies to identify key biomarkers and early signs of degenerative changes that lead to AD. |
Cell cycle protein kinases play pivotal roles in neuronal survival or death decisions in AD and other neurodegenerative diseases. These proteins initiate changes to chromatin structure (altered gene expression and opportunity for oxidative damage to DNA), phosphorylate proteins that can aggregate into pathologic lesions (tau), and directly induce apoptotic pathways of cell death. |
Additional animal models that induce cell cycle protein abnormalities in APP and tau transgenic mice. Also the use of cell cycle protein inhibitors in AD models to impede cell death. Such evidence is available in animal models of ALS. |
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