Linda Callahan
| Title | Research Assistant Professor |
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| Institution | School of Medicine and Dentistry |
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| Department | Pathology and Laboratory Medicine |
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| Address | University of Rochester Medical Center
School of Medicine and Dentistry
601 Elmwood Ave, Box 626
Rochester NY 14642
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| 1989 |
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| "Dean's Certificate and Prize for Excellence in Teaching", Albany Medical College Courses taught: Histology, Gross Anatomy | Albany Medical College | | 1990 |
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| Who's Who Among Students in American Universities and Colleges | | 1991 |
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| Albany Medical College Alumni Association Award | | 1994 |
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| Mary Notter Award for Excellence in Research | University of Rochester Medical Center | | 1997 |
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| NIH First Award (R29) | | 1998 |
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| Nominee, Student Employee Supervisor of the Year Award | | 2004 |
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| Invitation to Editorial Board, Journal of Neuropathology and Experimental Neurology |
Late-onset neurodegenerative diseases, including Alzheimer's disease (AD), Amyotrophic Lateral Sclerosis (ALS), and Parkinson's Disease (PD), are the result of abnormal function of specific populations of neurons within the central nervous system. The deficits leading to clinical symptomology include a progressive synapse loss within specific neuronal networks. The synapse loss is likely mediated in part by cell loss but also by synapse dysfunction. Numerous factors have been identified as synaptic degenerators, including disruption of the cytoskeletal network, particularly of the cytoskeletal proteins mediating axonal transport.
Our primary research interests focus on axonal transport disruption mediated by cytoskeletal protein alterations. We are particularly interested in the initial response of both effected and neighboring uneffected cells to events of cytoskeletal disruption. Ongoing research focuses on the response of neurons undergoing microtubule disruption. To this end, we use primary hippocampal neurons in co-culture to examine microtubule disruption due to nocodazole (a microtubule inhibitor drug) or pathogenic tau proteins, including P301L and R406W. We are also investigating effects of overexpression of normal four-repeat tau on microtubule patterns. We are embarking on the development of late-onset models which will express tau pathogenitors at the CNS location and time of choosing of the investigator. Our analyses are multi-faceted combining histological, immunocytochemical, ultrastructural, quantitative, and molecular biological techniques to analyze alterations resulting from cytoskeletal disruption.
Long-term research goals include: 1) to determine the initial response of cell defense systems (lysosomal, ubiquitin-proteasomal-system (UPS)) to disruption of cytoskeletal proteins (microtubules and neurofilaments in particular), 2) to determine the response of cell defense systems of near neighbor neurons (apparently uneffected), 3) to determine if similarities exist between the late-onset neurodegenerative diseases of Alzheimer's Disease, Amyotrophic Lateral Sclerosis, and Parkinson's Disease, in regards to the response of neurons undergoing cytoskeletal disruption, and 4) to create models which allow control over the CNS location and age of expression of cytoskeletal disruptors. The overall goal of our research is to mimic molecular cytoskeletal disruption, and to mechanistically dissect the response of both effected and neighboring uneffected neurons with an aim towards providing therapeutic targets.
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Muyan M, Callahan LM, Huang Y, Lee AJ. The ligand-mediated nuclear mobility and interaction with estrogen-responsive elements of estrogen receptors are subtype specific. J Mol Endocrinol. 2012; 49(3):249-66.
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Sharma A, Callahan LM, Sul JY, Kim TK, Barrett L, Kim M, Powers JM, Federoff H, Eberwine J. A neurotoxic phosphoform of Elk-1 associates with inclusions from multiple neurodegenerative diseases. PLoS One. 2010; 5(2):e9002.
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Staversky RJ, Vitiello PF, Yee M, Callahan LM, Dean DA, O'Reilly MA. Epithelial ablation of Bcl-XL increases sensitivity to oxygen without disrupting lung development. Am J Respir Cell Mol Biol. 2010 Sep; 43(3):376-85.
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Janelsins MC, Mastrangelo MA, Park KM, Sudol KL, Narrow WC, Oddo S, LaFerla FM, Callahan LM, Federoff HJ, Bowers WJ. Chronic neuron-specific tumor necrosis factor-alpha expression enhances the local inflammatory environment ultimately leading to neuronal death in 3xTg-AD mice. Am J Pathol. 2008 Dec; 173(6):1768-82.
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Luo Y, Henricksen LA, Giuliano RE, Prifti L, Callahan LM, Federoff HJ. VIP is a transcriptional target of Nurr1 in dopaminergic cells. Exp Neurol. 2007 Jan; 203(1):221-32.
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Miller RM, Callahan LM, Casaceli C, Chen L, Kiser GL, Chui B, Kaysser-Kranich TM, Sendera TJ, Palaniappan C, Federoff HJ. Dysregulation of gene expression in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mouse substantia nigra. J Neurosci. 2004 Aug 25; 24(34):7445-54.
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Callahan LM, Vaules WA, Coleman PD. Progressive reduction of synaptophysin message in single neurons in Alzheimer disease. J Neuropathol Exp Neurol. 2002 May; 61(5):384-95.
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Yermakova AV, Rollins J, Callahan LM, Rogers J, O'Banion MK. Cyclooxygenase-1 in human Alzheimer and control brain: quantitative analysis of expression by microglia and CA3 hippocampal neurons. J Neuropathol Exp Neurol. 1999 Nov; 58(11):1135-46.
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Callahan LM, Vaules WA, Coleman PD. Quantitative decrease in synaptophysin message expression and increase in cathepsin D message expression in Alzheimer disease neurons containing neurofibrillary tangles. J Neuropathol Exp Neurol. 1999 Mar; 58(3):275-87.
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Yao PJ, Morsch R, Callahan LM, Coleman PD. Changes in synaptic expression of clathrin assembly protein AP180 in Alzheimer's disease analysed by immunohistochemistry. Neuroscience. 1999; 94(2):389-94.
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Chow N, Cox C, Callahan LM, Weimer JM, Guo L, Coleman PD. Expression profiles of multiple genes in single neurons of Alzheimer's disease. Proc Natl Acad Sci U S A. 1998 Aug 4; 95(16):9620-5.
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Callahan LM, Chow N, Cheetham JE, Cox C, Coleman PD. Analysis of message expression in single neurons of Alzheimer's disease brain. Neurobiol Aging. 1998 Jan-Feb; 19(1 Suppl):S99-105.
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Callahan LM, Coleman PD. Neurons bearing neurofibrillary tangles are responsible for selected synaptic deficits in Alzheimer's disease. Neurobiol Aging. 1995 May-Jun; 16(3):311-4.
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Callahan LM, Selski DJ, Martzen MR, Cheetham JE, Coleman PD. Preliminary evidence: decreased GAP-43 message in tangle-bearing neurons relative to adjacent tangle-free neurons in Alzheimer's disease parahippocampal gyrus. Neurobiol Aging. 1994 May-Jun; 15(3):381-6.
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Mazurkiewicz JE, Callahan LM, Swash M, Martin JE, Messer A. Cytoplasmic inclusions in spinal neurons of the motor neuron degeneration (Mnd) mouse. I. Light microscopic analysis. J Neurol Sci. 1993 May; 116(1):59-66.
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Callahan LM, Wylen EL, Messer A, Mazurkiewicz JE. Neurofilament distribution is altered in the Mnd (motor neuron degeneration) mouse. J Neuropathol Exp Neurol. 1991 Jul; 50(4):491-504.
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Adler KB, Callahan LM, Evans JN. Cellular alterations in the alveolar wall in bleomycin-induced pulmonary fibrosis in rats. An ultrastructural morphometric study. Am Rev Respir Dis. 1986 Jun; 133(6):1043-8.
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Callahan LM, Evans JN, Adler KB. Alterations in the cellular population of the alveolar wall in an animal model of fibrosis. A morphometric study. Chest. 1986 Mar; 89(3 Suppl):188S-189S.
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