Tritia R. Yamasaki, MD, PhD

Practice areas

Practice areas

Clinical interests

  • Ataxia and Gait Disorders
  • Atypical Parkinsonism
  • Dystonia
  • Huntington's Disease
  • Movement Disorders including Tremor
  • Myoclonus
  • Parkinson's Disease
  • Restless Leg Syndrome

Awards

Alpha Omega Alpha - University of California, Irvine

Pathology Chairs Honor Society - University of California, Irvine

Sigma Xi Research Society - University of California, Irvine


Tritia R. Yamasaki, MD, PhD

Biography

Tritia Yamasaki, MD, received her medical and research degrees at the University of California, Irvine and trained in neurology at University of California, Los Angeles. She completed a fellowship in movement disorders at Washington University in St. Louis, School of Medicine. Yamasaki is board certified by the American Board of Psychiatry and Neurology in Neurology. She is also a member of the American Academy of Neurology and the International Parkinson and Movement Disorder Society.

Research focus

I am interested in research, and my lab studies the protein alpha-synuclein, which accumulates abnormally in Parkinson's disease as well as other diseases.

Faculty rank

Assistant Professor of Neurology

Education

Degree
University of California - Irvine

Residency
University of California - Los Angeles

Fellowship
Movement Disorders, Washington University in St. Louis, School of Medicine

Certifications or Special training
American Board of Psychiatry and Neurology, Neurology

Neurology

Kentucky Neuroscience Institute

Kentucky Clinic
First Floor, Wing C, Room B101
740 S. Limestone
Lexington KY 40536-0284

Call 859-323-5661
Fax 859-323-3753

Amenities
Dining, Internet/Wi-Fi, Information desk, Pharmacy services, Wheelchairs

Parking is available at the Kentucky Clinic Parking Garage (PS #3).

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1. Proteopathic tau seeding predicts tauopathy in vivo.
Holmes BB, Furman JL, Mahan TE, Yamasaki TR, Mirbaha H, Eades WC, Belaygorod L, Cairns NJ, Holtzman DM, Diamond MI.
Proc Natl Acad Sci U S A. 2014 Oct 14;111(41):E4376-85. doi: 10.1073/pnas.1411649111. Epub 2014 Sep 26.

2. Cerebrospinal fluid biomarkers in clinical subtypes of early-onset Alzheimer's disease.
Teng E, Yamasaki TR, Tran M, Hsiao JJ, Sultzer DL, Mendez MF.
Dement Geriatr Cogn Disord. 2014;37(5-6):307-14. doi: 10.1159/000355555. Epub 2013 Dec 31.

3. Neural stem cells improve cognition via BDNF in a transgenic model of Alzheimer disease.
Blurton-Jones M, Kitazawa M, Martinez-Coria H, Castello NA, Müller FJ, Loring JF, Yamasaki TR, Poon WW, Green KN, LaFerla FM.
Proc Natl Acad Sci U S A. 2009 Aug 11;106(32):13594-9. doi: 10.1073/pnas.0901402106. Epub 2009 Jul 24.

4. Activation of cell cycle proteins in transgenic mice in response to neuronal loss but not amyloid-beta and tau pathology.
Lopes JP, Blurton-Jones M, Yamasaki TR, Agostinho P, LaFerla FM.
J Alzheimers Dis. 2009;16(3):541-9. doi: 10.3233/JAD-2009-0993.

5. Neural stem cells improve memory in an inducible mouse model of neuronal loss.
Yamasaki TR, Blurton-Jones M, Morrissette DA, Kitazawa M, Oddo S, LaFerla FM.
J Neurosci. 2007 Oct 31;27(44):11925-33.

6. Lipopolysaccharide-induced inflammation exacerbates tau pathology by a cyclin-dependent kinase 5-mediated pathway in a transgenic model of Alzheimer's disease.
Kitazawa M, Oddo S, Yamasaki TR, Green KN, LaFerla FM.
J Neurosci. 2005 Sep 28;25(39):8843-53.

7. Microglia as a potential bridge between the amyloid beta-peptide and tau.
Kitazawa M, Yamasaki TR, LaFerla FM.
Ann N Y Acad Sci. 2004 Dec;1035:85-103. Review.

8. Inclusion body myositis-like phenotype induced by transgenic overexpression of beta APP in skeletal muscle.
Sugarman MC, Yamasaki TR, Oddo S, Echegoyen JC, Murphy MP, Golde TE, Jannatipour M, Leissring MA, LaFerla FM.
Proc Natl Acad Sci U S A. 2002 Apr 30;99(9):6334-9. Epub 2002 Apr 23.

9. Calsenilin reverses presenilin-mediated enhancement of calcium signaling.
Leissring MA, Yamasaki TR, Wasco W, Buxbaum JD, Parker I, LaFerla FM.
Proc Natl Acad Sci U S A. 2000 Jul 18;97(15):8590-3.