Trisha Stan is a fellow in the Program for Writing and Rhetoric and teaches science-themed writing and oral communication courses. She completed her Ph.D. in Immunology at Stanford University in 2014, in which she studied the interaction of the immune system and the brain in neurodegenerative disorders. She is a co-founder of the student-run science podcast Goggles Optional, for which she enjoys "improving" the lyrics to popular songs to make them about science.

Academic Appointments

  • Lecturer, Stanford Introductory Studies - Program in Writing and Rhetoric

Professional Education

  • B.A., William Jewell College, Oxbridge (Honors) Molecular Biology, Philosophy (2009)
  • Ph.D., Stanford University, Immunology (2014)

All Publications

  • Autoimmunity contributes to nociceptive sensitization in a mouse model of complex regional pain syndrome PAIN Li, W., Guo, T., Shi, X., Czirr, E., Stan, T., Sahbaie, P., Wyss-Coray, T., Kingery, W. S., Clark, J. D. 2014; 155 (11): 2377-2389
  • TDP-43 frontotemporal lobar degeneration and autoimmune disease JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY Miller, Z. A., Rankin, K. P., Graff-Radford, N. R., Takada, L. T., Sturm, V. E., Cleveland, C. M., Criswell, L. A., Jaeger, P. A., Stan, T., Heggeli, K. A., Hsu, S. C., Karydas, A., Khan, B. K., Grinberg, L. T., Gorno-Tempini, M. L., Boxer, A. L., Rosen, H. J., Kramer, J. H., Coppola, G., Geschwind, D. H., Rademakers, R., Seeley, W. W., Wyss-Coray, T., Miller, B. L. 2013; 84 (9): 956-962


    BACKGROUND: The aetiology and pathogenesis of non-genetic forms of frontotemporal dementia (FTD) is unknown and even with the genetic forms of FTD, pathogenesis remains elusive. Given the association between systemic inflammation and other neurodegenerative processes, links between autoimmunity and FTD need to be explored. OBJECTIVE: To describe the prevalence of systemic autoimmune disease in semantic variant primary progressive aphasia (svPPA), a clinical cohort, and in progranulin (PGRN) mutation carriers compared with neurologically healthy normal controls (NC) and Alzheimer's disease (AD) as dementia controls. DESIGN: Case control. SETTING: Academic medical centres. PARTICIPANTS: 129 svPPA, 39 PGRN, 186 NC and 158 AD patients underwent chart review for autoimmune conditions. A large subset of svPPA, PGRN and NC cohorts underwent serum analysis for tumour necrosis factor α (TNF-α) levels. OUTCOME MEASURES: χ(2) Comparison of autoimmune prevalence and follow-up logistic regression. RESULTS: There was a significantly increased risk of autoimmune disorders clustered around inflammatory arthritides, cutaneous disorders and gastrointestinal conditions in the svPPA and PGRN cohorts. Elevated TNF-α levels were observed in svPPA and PGRN compared with NC. CONCLUSIONS: svPPA and PGRN are associated with increased prevalence of specific and related autoimmune diseases compared with NC and AD. These findings suggest a unique pattern of systemic inflammation in svPPA and PGRN and open new research avenues for understanding and treating disorders associated with underlying transactive response DNA-binding protein 43 aggregation.

    View details for DOI 10.1136/jnnp-2012-304644

    View details for Web of Science ID 000323164000007

  • The ageing systemic milieu negatively regulates neurogenesis and cognitive function NATURE Villeda, S. A., Luo, J., Mosher, K. I., Zou, B., Britschgi, M., Bieri, G., Stan, T. M., Fainberg, N., Ding, Z., Eggel, A., Lucin, K. M., Czirr, E., Park, J., Couillard-Despres, S., Aigner, L., Li, G., Peskind, E. R., Kaye, J. A., Quinn, J. F., Galasko, D. R., Xie, X. S., Rando, T. A., Wyss-Coray, T. 2011; 477 (7362): 90-U157


    In the central nervous system, ageing results in a precipitous decline in adult neural stem/progenitor cells and neurogenesis, with concomitant impairments in cognitive functions. Interestingly, such impairments can be ameliorated through systemic perturbations such as exercise. Here, using heterochronic parabiosis we show that blood-borne factors present in the systemic milieu can inhibit or promote adult neurogenesis in an age-dependent fashion in mice. Accordingly, exposing a young mouse to an old systemic environment or to plasma from old mice decreased synaptic plasticity, and impaired contextual fear conditioning and spatial learning and memory. We identify chemokines--including CCL11 (also known as eotaxin)--the plasma levels of which correlate with reduced neurogenesis in heterochronic parabionts and aged mice, and the levels of which are increased in the plasma and cerebrospinal fluid of healthy ageing humans. Lastly, increasing peripheral CCL11 chemokine levels in vivo in young mice decreased adult neurogenesis and impaired learning and memory. Together our data indicate that the decline in neurogenesis and cognitive impairments observed during ageing can be in part attributed to changes in blood-borne factors.

    View details for DOI 10.1038/nature10357

    View details for Web of Science ID 000294404300037

    View details for PubMedID 21886162