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Tritia Yamasaki, MD, PhD



  • Associate Professor

College Unit(s)

Other Affiliation(s)
  • Neuroscience - Joint Faculty

Biography and Education


I received my B.S in biology from Yale University. I then trained in the Medical Scientist Training Program at University of California, Irvine, where I received my MD, and my PhD in the study of neurodegenerative disease. I then completed an internal medicine year at UCI, followed by a neurology fellowship at UCLA. I completed a two-year fellowship in movement disorders at Washington University St Louis where I was also a research fellow studying aggregation of the protein alpha-synuclein. I have been in the movement disorder group at University of Kentucky since 2015.


I study abnormal aggregation of the protein alpha-synuclein which accumulates abnormally in neurodegenerative diseases such as Parkinson's disease, multiple system atrophy, and Lewy body dementia.

Selected Publications

1. Holmes, B.H., Furman, J.L., Mahan, T., Yamasaki, T.R., Eades, W.C., Belaygorod, L., Cairns, N.J., Holtzman, D.M., and Diamond M.I. (2014). Proteopathic tau seeding predicts tauopathy in vivo. Proceedings of the National Academy of Sciences, U.S.A. 111(41), E4376-85. 2. Teng, E., Yamasaki, T.R., Tran, M., Hsiao, J.J., Sultzer, D.L., and Mendez, M.F (2013). Cerebrospinal fluid biomarkers in clinical subtypes of Early-Onset Alzheimer’s Disease. Dementia Geriatric Cognitive Disorders, 37 (5-6): 307-314. 3. Rao, N.M., Yamasaki, T., Mishra, S.K., and Yim, C. (2013). Variant lateral medullary syndrome in a patient presenting with inability to swallow. Neurohospitalist, 3 (2): 98-9. 4. Blurton-Jones, M., Kitazawa, M., Martinez-Coria, H., Castello, N., Muller, F.J., Loring, J.F., Yamasaki , T.R., Poon, W.W., Green K.N, and LaFerla, F.M. (2009). Neural stem cells improve cognition via BDNF in a transgenic model of Alzheimer disease. Proceedings of the National Academy of Sciences, U.S.A. 106, 13594-9. 5. Lopes, J.P., Blurton-Jones, M., Yamasaki T.R., Agostinho, P., LaFerla, F.M. (2009) Activation of cell cycle proteins in transgenic mice in response to neuronal loss but not amyloid-beta and tau pathology. Journal of Alzheimers Disease. 16(3), 541-9. 6. Yamasaki, T.R., Blurton-Jones, M., Morrissette, D.H., Kitazawa, M., Oddo, S., and LaFerla, F.M. (2007). Neural stem cells improve memory in an inducible mouse model of neuronal loss. Journal of Neuroscience 44, 11925-33. 7. Kitazawa, M., Oddo, S., Yamasaki, T.R., Green, K., and LaFerla, F.M. (2005). Lipopolysaccharide-induced inflammation exacerbates tau pathology by a cyclin-dependent kinase 5-mediated pathway in a transgenic model of Alzheimer's disease. Journal of Neuroscience. 39, 8843-53. 8. Kitazawa, M., Yamasaki, T.R., and LaFerla, F.M. (2004). Microglia as a potential bridge between the amyloid  peptide and tau. Annals of the New York Academy of Sciences. 1035, 85-103. 9. Sugarman, M.C., Yamasaki, T.R., Oddo, S., Echegoyen, J.C., Murphy, M.P., Golde, T.E., Jannatipour, M., Leissring, M.A., and LaFerla, F.M. (2002). Inclusion body myositis-like phenotype induced by transgenic overexpression of -APP in skeletal muscle. Proceedings of the National Academy of Sciences, U.S.A. 99, 6334-9. 10. Leissring, M.A., Yamasaki, T.R., Wasco, W., Buxbaum, J.D., Parker, I., and LaFerla, F.M. (2000). Calsenilin reverses presenilin-mediated enhancement of calcium signaling. Proceedings of the National Academy of Sciences, U.S.A.. 97, 8590-3.

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