George Bloom

Professor of Biology, Cell Biology, and Neuroscience, Chair of Biology
216 PLSB
(434) 243-3543
Lab: (434) 243-7764

Education

  • B.A., University of Pennsylvania, 1973
  • Ph.D., University of Pennsylvania, 1979

Research Interests

Research in our laboratory is now focused primarily on Alzheimer’s disease (AD). The histopathological hallmark of AD is the presence in brain of extracellular plaques of ß-amyloid peptide fibrils, and intraneuronal neurofibrillary tangles, which are filaments composed of the protein, tau. Despite the conspicuous appearance of plaques and tangles, a growing body of evidence points to their building blocks, ß-amyloid and tau oligomers, as being the toxic molecular species that cause AD. For example, we have found that tau expression is required for several adverse effects of ß-amyloid oligomers on neurons, including microtubules loss, ectopic re-rentry into the cell cycle and cytotoxicity. The goals of our work are to decipher the metabolic links that connect ß-amyloid and tau to damage neurons, to define the structures and pathological properties of various types of ß-amyloid and tau oligomers, and to develop effective therapeutic and diagnostic tools for AD.
 

 

 

For more information about research interests, visit my lab website.

Representative Publications

  • Norambuena, A., Wallrabe, H., McMahon, L., Silva, A., Swanson, E., Thomas, S,. Baerthlein, D., Kodis, E., Oddo, S., Mandell, J.W. and Bloom, G.S. (2017). mTOR and neuronal cell cycle reentry:How Impaired Brain Insulin Signaling Promotes Alzheimer’s Disease. Alzheimer’s & Dementia, 13: 152-167.    
     
  • Sharlow, E.R., Leimgruber, S., Lira, A., McConnell, M.J., Saucerman, J.J., Brautigan, D.L., Kubicka, E., Norambuena, A., Bloom, G.S., Epperly, M.W., Greenberger, J.S. and Lazo, J.S. (2016). A small molecule screen exposes mTOR signaling pathway involvement in radiation-induced apoptosis. ACS Chemical Biology, 11: 1428-1437. 
     
  • Khan, S.S. and Bloom, G.S. (2016). Tau: The Center of a Signaling Nexus in Alzheimer’s Disease. Frontiers in Neuroscience, 10: article 31. PMCID: PMC4746348.
     
  • Fang, X., Bianhong, Z., Thisse, B., Bloom, G.S. and Thisse, C. (2015). IQGAP3 Is Essential for Cell Proliferation and Motility During Zebrafish Embryonic Development. Cytoskeleton 72: 422-433. PMCID: PMC4600665.
     
  • Marbiah, M., Harvey, A., West, B., Louzolo, A., Banerjee, P., Alden, J., Grigoriadis, A., Hummerich, H., Kan, H-M., Cai, Y., Bloom, G.S., Parmjit, J., Collinge, J. and Klöhn, P-C. (2014). Identification of a Gene Regulatory Network Associated with Prion Replication. EMBO Journal, 33: 1527-1547. PMCID:PMC4198050.
     
  • Bloom, G.S. (2014). Amyloid and Tau: the Trigger and Bullet in Alzheimer's Disease Pathogenesis JAMA Neurology, 71: 505-508. PMCID-in process. 
     
  • Wallrabe, H., Cai, Y., Sun, Y., Perisasamy, A., Schafer, D.A., Kan, H-M., Pereira, R.L., and Bloom, G.S. (2013). IQGAP1 Interactome Analysis by In Vitro Reconstitution and Live Cell 3-Color FRET Microscopy. Cytoskeleton, 70: 819-836. PMCID: PMC3917506.