Michelle L. Steinhilb

Photo of Michelle SteinhilbAssociate Professor
Brooks Hall 206A (Office)
Brooks Hall 206 (Lab)
  • B.S., Wayne State University, 1996
  • Ph.D., University of Michigan, 2002
  • Postdoc, Harvard Medical School, 2002-2006
Teaching Areas
Genetics, Biotechnology, Neuroscience
Research Fields
Genetic models of human neurodegenerative disease, cellular and molecular neurobiology
​​Current Research Projects
Research in my lab focuses on understanding the underlying causes of Alzheimer’s disease using the powerful molecular and genetic tools available in the model organism Drosophila melanogaster (the fruit fly). Alzheimer’s disease belongs to a group of related disorders known as “tauopathies” whose common pathology involves tau, a microtubule-associated protein that is highly abundant in neurons. Normally, tau physically interacts with microtubules to help cells maintain their shape and transport critical substances to cellular locations where they are needed. Alzheimer’s disease conditions, however, lead to a breakdown of normal tau function. To investigate the role of tau in disease, our lab uses several approaches, including Drosophila genetics, tissue culture, molecular biology, biochemistry, and microscopy. We hope to ultimately learn more about the underlying causes of tau toxicity in order to help others to develop new treatment strategies to prevent or cure Alzheimer’s disease.
Selected Publications
  • Steinhilb ML, Dias-Santagata D, Fulga TA, Felch DL, Feany MB.  Tau phosphorylation sites work in concert to promote neurotoxicity in vivo Molecular Biology of the Cell (2007) Dec; 18(12): 5060-8. 
  • Steinhilb ML, Dias-Santagata D, Mulkearns EE, Shulman JM, Biernat J, Mandelkow EM, Feany MB.  S/P and T/P phosphorylation is critical for tau neurotoxicity in Drosophila.                  Journal of Neuroscience Research (2007) May 1; 85(6): 1271-8. 
  • Fulga TA, Elson-Schwab I, Khurana V, Steinhilb ML, Spires TL, Hyman BT, Feany MB.  Abnormal bundling and accumulation of F-actin mediates tau-induced neuronal degeneration in vivo.  Nature Cell Biology (2007) Feb; 9(2): 139-48. 
  • Khurana V, Lu Y, Steinhilb ML, Oldham S, Shulman JM, Feany MB. TOR-mediated cell cycle activation causes neurodegeneration in a Drosophila tauopathy model.  Current Biology (2006) Feb 7; 16(3): 230-41. 
  • Steinhilb ML, Turner RS, Gaut JR. ELISA analysis of beta-secretase cleavage of the Swedish amyloid precursor protein in the secretory and endocytic pathways.   Journal of Neurochemistry (2002) Mar; 80(6): 1019-28. 
  • Steinhilb ML, Turner RS, and Gaut JR. The protease inhibitor, MG132, blocks maturation of the amyloid precursor protein Swedish mutant preventing cleavage by beta-secretase.   Journal of Biological Chemistry (2001) Feb 9; 276(6): 4476-84.