Bio

Jessie Ong is a 2026 Ellison Scholar, a current BS/MS student in Biology at Stanford, and an incoming DPhil student in Paediatrics at the University of Oxford focused on vaccine discovery. Her research spans immunology, synthetic biology, and neuroscience, with experience across the University of Oxford, Stanford, and the Italian Institute of Technology. She is interested in leveraging disease heterogeneity to develop clinically translatable, scalable vaccines that minimize resistance.

Honors & Awards

  • 2026 Ellison Scholarship, DPhil in Paediatrics, Ellison Institute of Technology, University of Oxford (2026)
  • Stanford Major Grant Awardee, Stanford Vice Provost for Undergraduate Education (June 2025)
  • Stanford Global Studies Summer Fellow, Stanford Global Studies
  • Bio-X Undergraduate Fellow, Stanford Bio-X (June 2024)
  • Haas Center Community Service Fellow, Haas Center for Public Service (June 2024)

Professional Affiliations and Activities

  • Speaker, TEDxStanford (2025 - 2025)
  • Bio-X Undergraduate Fellow, Stanford BioX (2024 - 2024)
  • Board Member, Stanford Down Syndrome Research Center (2023 - Present)

Contact

  • Academic
    jessieo@stanford.edu
    University - Student Department: Biology Position: Undergraduate
    University - Student Department: Biology Position: Graduate

Additional Info

  • Mail Code: 5020

Current Research and Scholarly Interests

Under mentorship of Jennifer Anne Co (PhD Candidate) in the Steven Banik Lab.
Engineering a molecular-glue detector in mammalian cells with CRISPR and degron based tools.
Creating platform for novel drug candidates through screening of a 15,000 protein ORFeome library.

All Publications

  • Selectively Blocking Small Conductance Ca2+-Activated K+ Channels Improves Cognition in Aged Mice. Biology Ong, J., Heller, H. C., Pittaras, E. 2025; 14 (2)

    Abstract

    Aging is associated with decreased neuronal sensitivity and activity that creates deficits in cognitive processes, including learning, memory, motivation, general activity, and other behaviors. These effects are due in part to decreased intracellular Ca2+ homeostasis, increasing hyperpolarization of the resting potential in aged neurons and therefore decreasing their excitability. To reduce hyperpolarization in aged mice, we used apamin, a selective small conductance Ca2+-activated K+ (sKCa) channel blocker. By blocking the sKCa channels, apamin decreases the egress of the K+ out of the cell, reducing its hyperpolarization and causing it to be closer to threshold potential. As a result, neurons should be more sensitive to excitatory stimuli and more active. We evaluated the performance of aged mice in a selection of cognitive and behavioral tests prior to and after systemic applications of apamin or the vehicle saline. Apamin improved performance in short-term memory, increased attention to tasks, and decreased anhedonia. Apamin had no significant effect on long-term spatial and recognition memory, risk-taking behavior, sociability, and anxiety. Our results are compatible with the known effects of sKCa channel blockade on neuronal sensitivity and activity; however, these short-term effects were not reflected in longer-term alterations of neural plasticity responsible for long-term spatial and recognition memory or other more complex cognitive processes we evaluated.

    View details for DOI 10.3390/biology14020149

    View details for PubMedID 40001917

    View details for PubMedCentralID PMC11851921