Albee Messing

messing@waisman.wisc.edu

Department of Comparative Biosciences
Office: WAISMAN CTR

Albee Messing

Titles and Education

  1. BS 1974, Yale College
  2. VMD 1978, University of Pennsylvania
  3. PhD 1982, University of Pennsylvania

Research

Research in my laboratory is directed at understanding developmental and pathologic aspects of neuronal and glial cell biology in the nervous system of the mouse, and genetic analysis of a human disorder of astrocytes, Alexander disease. 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. Most of our effort is directed at understanding the role of GFAP, the astrocyte-specific intermediate filament, in astrocyte development and reaction to injury in the central nervous system, and the mechanisms by which GFAP mutations lead to Alexander disease. We are also trying to identify biomarkers for tracking the clinical course of Alexander disease patients, and devise therapies for this disorder.

Responsibilities

Professor

  • Veterinary Histology 934:501 (Co-Coordinator)
  • Director, Rodent Models Core, Waisman Center

Clinical Interests

Alexander disease
CSF analysis

Recent Publications

  1. Messing, A., Li, R., Naidu, S., Taylor, J.P., Silverman, L., Flint, D., van der Knaap, M.S., and Brenner, M. (2012). Archetypal and new families with Alexander disease and novel mutations in GFAP. Archives of Neurology 69, 208-214.
  2. Messing, A., Brenner, M., Feany, M.B., Nedergaard, M., and Goldman, J.E. (2012). Alexander disease. Journal of Neuroscience 32, 5017-5023.
  3. Hagemann, T.L., Boelens, W., Wawrousek, E., and Messing, A. (2009). Suppression of GFAP toxicity by αB-crystallin in mouse models of Alexander disease. Human Molecular Genetics 18, 1190-1199.
  4. Hagemann TL, Connor JX, & Messing A. Alexander disease-associated GFAP mutations in mice induce Rosenthal fiber formation and a white matter stress response. Journal of Neuroscience 26:11162-11173, 2006.
  5. Brenner M, Johnson AB, Boespflug-Tanguy O, Rodriguez D, Goldman JE, & MESSING A. Mutations in GFAP, encoding glial fibrillary acidic protein, are associated with Alexander disease. Nature Genetics 27:117-120, 2001.