
Albee Messing
VMD, PhD, University of Pennsylvania
Faculty Core Director, Rodent Models Core
Professor, Comparative Biosciences
Contact Information:
Waisman Center
UW-Madison
1500 Highland Avenue
Madison, WI 53705
Phone: (608) 263-9191
Fax: (608) 263-4364
E-mail: messing@waisman.wisc.edu
Web: Alexander Disease
Research in my laboratory is directed at understanding developmental and pathologic aspects of glial cell biology in the nervous system of the mouse, with a particular focus on astrocytes and their major intermediate filament protein, GFAP. Our main strategies involve genetic manipulation of glial gene expression using transgenic techniques, and gene targeting in embryonic stem cells, to generate mutant strains of mice. Current projects address a variety of topics such as regulation of gene expression, the role of GFAP mutations and accumulation in the pathogenesis of Alexander disease. A major effort is devoted to devising novel therapeutic strategies for treatment of this disorder, and identifying biomarkers to permit monitoring severity or progression of the disease.
Brenner M, Johnson AB, Boespflug-Tanguy O, Rodriguez D, Goldman JE, & MESSING A.(2001) Mutations in GFAP, encoding glial fibrillary acidic protein, are associated with Alexander disease. Nature Genet. 27:117-120. PMID: 11138011
Hagemann TL, Gaeta SA, Smith MA, Johnson DA, Johnson JA, Messing A. (2005). Gene expression analysis in mice with elevated glial fibrillary acidic protein and Rosenthal fibers reveals a stress response followed by glial activation and neuronal dysfunction. Hum Mol Genet, 14, 2443-2458. PMID: 16014634
Li R, Johnson AB, Salomons G, Goldman JE, Naidu S, Quinlan R, Cree B, Ruyle SZ, Banwell B, D'Hooghe M, Siebert JR, Rolf CM, Cox H, Reddy A, Gutierrez-Solana LG, Collins A, Weller RO, Messing A, van der Knaap MS, Brenner, M. (2005). Glial fibrillary acidic protein mutations in infantile, juvenile, and adult forms of Alexander disease. Ann Neurol, 57, 310-326. PMID: 15732097
Hagemann TL, Connor JX, Messing A. (2006). Alexander disease-associated GFAP mutations in mice induce Rosenthal fiber formation and a white matter stress response. J Neurosci, 26, 11162-11173. PMID:17065456
Cho W, Messing A. (2009). Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice. Exp Cell Res 315, 1260-1272. PMC2665202 PMID: 19146851
Hagemann TL, Boelens W, Wawrousek E, Messing A. (2009). Suppression of GFAP toxicity by αB-crystallin in mouse models of Alexander disease. Hum Mol Genet 18, 1190-1199. PMC2655774
Cho W, Hagemann TL, Johnson DA, Johnson JA, Messing A. (2009). Dual transgenic reporter mice as a tool for monitoring expression of GFAP. J Neurochem 110, 343-351. PMC2710392 PMID: 19457099
Cho W, Brenner M, Peters N, Messing A. (2010). Drug screening to identify suppressors of GFAP expression. Hum Mol Genet 19, 3169-3178. PMC2908470 PMID: 20538881
Messing A, Li R, Naidu S, Taylor JP, Silverman L, Flint D, van der Knaap MS, Brenner M. Archetypal and new families with Alexander disease and novel mutations in GFAP. Arch Neurol 69, 208-214. PMID:21987397
Reviews
Liem RKH, Messing A. Dysfunctions of neuronal and glial intermediate filaments in disease. Journal of Clinical Investigation 119, 1814-1824. PMC2701870
Messing A, LaPash Daniels CM, Hagemann TL. (2010) Strategies for treatment in Alexander disease. Neurotherapeutics 7, 507-515. PMC2948554
Video:
Why Rare Diseases Matter: The Changing Spectrum of Alexander Disease
Presented 02/02/2012
Department of Pediatrics Grand Rounds
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