Dr. Anderson performed his graduate work studying developmental neurobiology utilizing Drosophila. During his postdoctoral studies with Dr. John his research focused on the mechanisms causing glaucoma in DBA/2J mice. These mice develop a pigment liberating iris disease and a form of glaucoma resembling human pigmentary glaucoma. Using genetic approaches, two genes were identified (Gpnmb and Tyrp1) that play early roles in this disease. Both of these genes encode melanosomal proteins.
These findings suggested that a key aspect of pigmentary glaucoma in DBA/2J mice involves aberrant melanosomal processes affecting the toxic intermediates of melanin production. In the course of studying modifiers of the DBA/2J form of glaucoma, Dr. Anderson's research also found that immune reactions contribute to the anterior chamber disease of DBA/2J mice and with other lab members showed that bone marrow transfers confer a striking neuroprotection against this form of glaucoma.
Dr. Anderson is currently a member of the Departments of Molecular Physiology & Biophysics and Ophthalmology & Visual Sciences at the University of Iowa. His ongoing work continues to capitalize on the basic genetic skills of his past training, utilizing mouse genetics to provide and test unique hypotheses of ocular disease and now supplemented by clinical and human genetic resources at The University of Iowa. His email is email@example.com.
Howell GR, Libby RT, Marchant JK, Wilson LA, Cosma IM, Smith RS, Anderson MG, John SWM. 2007. Absence of glaucoma in DBA/2J mice homozygous for wild-type versions of Gpnmb and Tyrp1. BMC Genet 8:45
Anderson MG, Libby RT, Mao M, Cosma IM, Wilson LA, Smith RS, John SWM. 2006. Genetic context determines susceptibility to intraocular pressure elevation in a mouse pigmentary glaucoma. BMC Biol 4:20 http://www.biomedcentral.com/content/pdf/1741-7007-4-20.pdf
Anderson MG, Haraszti T, Petersen GE, Wirick S, Jacobsen C, John SWM, Grunze M. 2006. Scanning transmission X-ray microscopic analysis of purified melanosomes of the mouse iris. Micron 37: 689-698
Libby RT, Anderson MG, Pang I-H, Robinson Z, Savinova OV, Cosma IM, Snow A, Wilson LA, Smith RS, Clark AF, John SWM. 2005. Inherited glaucoma in DBA/2J mice: pertinent disease features for studying the neurodegeneration. Vis Neurosci 22: 637-648
Anderson MG, Libby RT, Gould DB, Smith RS, John SWM. 2005. High-dose radiation with bone marrow transfer prevents neurodegeneration in an inherited glaucoma. Proc Natl Acad Sci USA 102: 4566-4571 http://www.pnas.org/cgi/content/full/102/12/4566
Mo JS, Anderson MG, Gregory M, Smith RS, Savinova OV, Serreze DV, Ksander BR, Streilein JW, John SWM. 2003. By altering ocular immune privilege, bone marrow-derived cells pathogenically contribute to DBA/2J pigmentary glaucoma. J Exp Med 197: 1335-1344
Anderson MG, Smith RS, Hawes NL, Zabaleta A, Chang B, Wiggs JL, John SWM. 2002. Mutations in genes encoding melanosomal proteins cause pigmentary glaucoma in DBA/2J mice. Nat Genet 30: 81-85
Anderson MG, Smith RS, Savinova OV, Hawes NL, Chang B, Zabaleta A, Wilpan R, Heckenlively JR, Davisson MT, John SWM. 2001. Genetic modification of glaucoma associated phenotypes between AKXD-28/Ty and DBA/2J mice. BMC Genetics 2: 1 http://www.biomedcentral.com/1471-2156/2/1
Chang B, Smith RS, Hawes NL, Anderson MG, Zabaleta A, Savinova O, Roderick TH, Heckenlively JR, Davisson MT, John SWM. 1999. Interacting loci cause severe iris atrophy and glaucoma in DBA/2J mice. Nat Genet 21: 405-409
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