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Dr. Jada Lewis

Modeling and Therapeutic Trials for Neurodegenerative Diseases: Alzheimer’s and Parkinson’s Diseases, Frontotemporal Dementia, and Amyotrophic Lateral Sclerosis

Associate Professor of Neuroscience;
Investigator, CTRND and McKnight Brain Institute
Post Doc, Neuroscience (Mike Hutton), Mayo Clinic, 1998-2000
Post Doc, Pharmacology (Ryzard Kole), University of North Carolina, Chapel Hill, 1996-1998
Ph.D., Genetics and Molecular Biology, University of North Carolina, Chapel Hill, 1992-1996
B.A., College Scholars with Emphasis in Genetics, University of Tennessee, 1989-1992
Contact Dr. Lewis
Phone: 352-273-9666

Research Focus and Aims
Our overall goal is to develop a better understanding of the processes that occur during neurodegenerative disorders in order to facilitate therapies that may ultimately prolong cognitive or motor function in diseases such as Alzheimer’s (AD) and Parkinson’s diseases (PD), frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). Additionally, we also are exploring the links between lysosomal storage diseases and neurodegenerative diseases of aging, including frontotemporal dementia and Parkinson’s Disease. A large part of our work involves the generation of constitutive and inducible model systems for the study of proteins that are thought to play a major role in disease progression including tau, TDP-43,and LRRK2. These models comprise a critical resource for the CTRND as it strives to translate laboratory findings into diagnostics or therapies for human diseases. In particular, we focus on cellular pathways altered in these mouse models that may play a contributory role in disease and study the formation of pathological species of protein that are hallmarks of the human condition. Understanding these pathways is key to developing therapies against these pathological proteins or the damage that they cause. In addition to our generation and characterization of novel model systems for human neurodegenerative diseases, we interact with other academic or pharmaceutical colleagues to determine the efficiency of novel therapies for the human diseases that we study. Recent funding from the NIH (NINDS, NIA), DoD, ALSA, Alzheimer’s Association, and MJFF. Private benefactors have also been critical in helping our studies move toward the clinic.

Ongoing projects in my laboratory include:

  1. Generation of models of FTD and ALS to understand how changes to Matrin3, TDP-43 and/or proganulin cause human disease.
  2. Utilizing our novel models for FTD and AD to understand how the tau protein causes and to identify ways through which the brain can be repaired
  3. Investigating the link between lysosomal storage disease that affect young adults and neurodegenerative disease of aging, with a focus on FTD and PD>
  4. Understanding how various genes or the encoded proteins can lead to the variable presentations of different neurodegenerative diseases

Each of these projects represents collaborations between my lab and other members of the CTRND including Dr. Borchelt, Giasson, Golde, and Rodriguez.

Join the team!


Selected Publications


  • Bailey RM, Howard J, Knight J, Sahara N, Dickson DW, and Lewis J. 2014. Effects of the C57BL/6 strain background on tauopathy progression in the rTg4510 mouse model. Molecular Neurodegeneration. 9: 8.
  • D’Alton S, Altshuler M, Cannon A, Dickson DW, Petrucelli L, and Lewis J.. 2014. Divergent phenotypes in mutant TDP-43 transgenic mice highlight potential confounds in TDP-43 transgenic modeling. PLoS One. 9(1): e86513.
  • Bailey RM, Covy JP, Melrose HL, Rousseau L, Watkinson R, Knight J, Miles S, Farrer MJ, Dickson DW, Giasson BI, and Lewis J. 2013. LRRK2 phosphorylates novel tau epitopes and promotes tauopathy. Acta Neuropathologica. 126(6): 809-827.
  • Clippinger AK, D’Alton S, Lin WL, Gendron TF, Howard J, Borchelt DR, Cannon A, Carlomagno Y, Chakrabarty P, Cook C, Golde TE, Levites Y, Ranum L, Schultheis PJ, Xu G, Petrucelli L, Sahara N, Dickson DW, Giasson B, and Lewis J. 2013. Robust cytoplasmic accumulation of phosphorylated TDP-43 in transgenic models of tauopathy. Acta Neuropathologica. 126(1): 39-50.
  • Rutherford NJ, Lewis J, Clippinger AK, Thomas MA, Adamson J, Cruz PE, Cannon A, Xu G, Golde TE, Shaw G, Borchelt DR, and Giasson BI. 2013. Unbiased screen reveals ubiquilin-1 and -2 highly associated with huntingtin inclusions. Brain Research. 1524: 62-73.
  • Cannon A, Yang B, Knight J, Farnham IM, Zhang Y, Wuertzer CA, D’Alton S, Lin WL, Castanedes-Casey M, Rousseau L, Scott B, Jurasic M, Howard J, Yu X, Bailey R, Sarkisian MR, Dickson DW, Petrucelli L, and Lewis J. 2012. Neuronal sensitivity to TDP-43 overexpression is dependent on timing of induction. Acta Neuropathologica. 123(6): 807-823.
  • Ahmed Z, Sheng H, Xu YF, Lin WL, Innes AE, Gass J, Yu X, Wuertzer CA, Hou H, Chiba S, Yamanouchi K, Leissring M, Petrucelli L, Nishihara M, Hutton ML, McGowan E, Dickson DW, and Lewis J. 2010. Accelerated lipofuscinosis and ubiquitination in granulin knockout mice suggest a role for progranulin in successful aging. American Journal of Pathology. 177(1): 311-324.

PubMed hyperlink