Elizabeth Thomas, PhD
Research Focus
Molecular Mechanisms of Neurological Disorders
Neurodegenerative Diseases
My current research program seeks to translate findings from gene expression studies into hypotheses about the pathological bases of neurological disorders, including schizophrenia and Huntington’s disease, as well as the mechanisms of drugs used to treat these disorders. We have used functional genomics approaches to identify genes that are abnormally expressed in human post-mortem samples from diseased subjects, animal models of disease and in response to drug treatment. The goal of these studies is to achieve a better understanding of dysfunctional systems in these disorders and to provide a basis for new therapeutic approaches and disease prevention.
Education
Ph.D. (Pharmacology), University of California, Irvine, 1994B.S. (Biology), University of California, Berkeley, 1989
Professional Experience
2013-2017 Associate Professor, Molecular and Cellular Neuroscience (MCN), Scripps Research2009-2012 Associate Professor, Molecular Biology, Scripps Research
2002-2009 Assistant Professor, Molecular Biology, Scripps Research
1998-2002 Senior Research Associate, Molecular Biology, Scripps Research
1995-1998 Research Associate, Molecular Biology, Scripps Research
Awards & Professional Activities
1992/1993 Henry Wood Elliot Memorial Award/Scholarship, The Univ. of California
1992-1994 PMAF Advanced Pre-doctoral Fellowship
1997-1999 NARSAD Young Investigator Fellowship
2001 Young Investigator Award, American Society for Neurochemistry
2002 The International Union of Basic and Clinical Pharmacology (IUPHAR) Young Investigator
Selected References
Mirendil, H., Thomas, E.A., De Leora, C., Okada, K., Inomata, Y., Chun, J. LPA signaling initiates schizophrenia-like brain and behavioral changes in a mouse model of prenatal brain hemorrhage. Translational Psychiatry 5: e541 (2015)
Jia, H., Morris, C.D., Williams, R., Loring, J.F., Thomas, E.A. Histone deacetylase inhibition imparts beneficial transgenerational epigenetic effects in Huntington's disease transgenic mice via alterations in DNA and histone methylation. Proc. Natl. Acad. Sci. USA 112(1):E56-64 (2015)
Thomas, E.A. Involvement of HDAC1 and HDAC3 in the pathology of polyglutamine disorders: therapeutic implications for selective HDAC1/HDAC3 inhibitors. Pharmaceuticals 7:634-661 (2014)
Tang, B, Jia, H., Kast, R. J., Thomas, E. A. Epigenetic changes at gene promoters in response to immune activation in utero. Brain, Behavior and Immunity. 30:168-75 (2013).
Jia, H., Kast, R. J., Steffan, J. S., Thomas, E. A. Selective histone deacetylase (HDAC) inhibition imparts beneficial effects in Huntington’s disease mice; implications for the ubiquitin–proteasomal and autophagy systems. Human Molecular Genetics, 21:5280-93 (2012).
Tang, B., Becanovic, K., Desplats, P.A., Spencer, B., Hill, A.M., Connolly, C., Masliah, E., Leavitt, B.R., Thomas, E.A. Forkhead box protein p1 is a transcriptional repressor of immune signaling in the CNS; implications for transcriptional dysregulation in Huntington disease. Human Molecular Genetics, 21:3097-111 (2012).
Jia, H., Pallos, J, Jacques, V., Lau, A., Tang, B., Cooper, A., Syed, A., Purcell, J., Chen, Y., Sharma, S., Sangrey, G.R., Darnell, S.B., Plasterer, H., Sadri-Vakili, G., Gottesfeld, J.M., Thompson, L.M., Rusche, J.R., Marsh, J.L., Thomas, E.A. Histone deacetylase (HDAC) inhibitors targeting HDAC3 and HDAC1 ameliorate polyglutamine-elicited phenotypes in model systems of Huntington's disease. Neurobiology of Disease, 46:351-61 (2012).
Tang, B., Dean, B., Thomas, E.A. Disease- and age-related changes in histone acetylation at gene promoters in psychiatric disorders. Translational Psychiatry, 1: e64 (2011). * this article was the #1 downloaded article for Translational Psychiatry in January 2012.
Thomas, E.A., Coppola, G., Tang, B., Kuhn, A., Kim, S., Geschwind, D.H., Brown, T.B., Luthi-Carter, R.,. Ehrlich, M.E. In Vivo Cell-autonomous Transcriptional Abnormalities Revealed in Mice Expressing Forebrain Striatal-restricted Mutant Huntingtin. Human Molecular Genetics, 2010 Dec. 20. * this article was featured on the cover.
Ku, S., Soragni, E., Campau, E., Thomas, E.A., Altun, G., Laurent, L.C., Loring, J.F., Napierala, M., Gottesfeld, J.M. Friedreich's Ataxia Induced Pluripotent Stem cells Model Intergenerational GAA*TTC Triplet-Repeat Instability. Cell Stem Cell 7(5):631-7 (2010).
Torkamani, A., Dean, B., Schork, N.J., Thomas, E.A. Co-Expression Network Analysis of Neural Tissue Reveals Perturbations in Developmental Processes in Schizophrenia. Genome Research, 20:403-12 (2010). * this article was featured on the cover.
Tang, B., Chang, W., Lanigan, C.M., Dean, B., Sutcliffe J.G., Thomas, E.A. Normal Human Aging and Early-Stage Schizophrenia Share Common Molecular Profiles. Aging Cell 8:339-42 (2009).
Thomas, E.A., Coppola, G., Desplats, P.A. Tang, B., Soragni, E. Burnett, R., Gao, F., Fitzgerald, K.M., Borok, J.F., Herman, D., Geschwind, D. H., Gottesfeld, J.M. The Histone Deacetylase Inhibitor, HDACi 4b, Ameliorates the Disease Phenotype and Transcriptional Abnormalities in Huntington's Disease Transgenic Mice. Proc. Natl. Acad. Sci. USA 105:15564-9 (2008).
Links
Team Reverses Huntington's Disease Symptoms in Mice
Scientists Identify Age-Associated Defects in Schizophrenia
Scripps Research Scientists Discover a Brain Cell Malfunction in Schizophrenia
Researchers Find Drug That Helps Huntington's Disease-Afflicted Mice-and Their Offspring
TSRI Scientists Find Molecular Trigger of Schizophrenia-Like Behaviors and Brain Changes