Professional Education

  • Doctor of Veterinary Medicine, Cornell University (2019)
  • Bachelor of Science, University of California Los Angeles (2012)

Stanford Advisors


All Publications

  • Cross-species translation of the Morris maze for Alzheimer's disease JOURNAL OF CLINICAL INVESTIGATION Possin, K. L., Sanchez, P. E., Anderson-Bergman, C., Fernandez, R., Kerchner, G. A., Johnson, E. T., Davis, A., Lo, I., Bott, N. T., Kiely, T., Fenesy, M. C., Miller, B. L., Kramer, J. H., Finkbeiner, S. 2016; 126 (2): 779-783


    Analogous behavioral assays are needed across animal models and human patients to improve translational research. Here, we examined the extent to which performance in the Morris water maze - the most frequently used behavioral assay of spatial learning and memory in rodents - translates to humans. We designed a virtual version of the assay for human subjects that includes the visible-target training, hidden-target learning, and probe trials that are typically administered in the mouse version. We compared transgenic mice that express human amyloid precursor protein (hAPP) and patients with mild cognitive impairment due to Alzheimer's disease (MCI-AD) to evaluate the sensitivity of performance measures in detecting deficits. Patients performed normally during visible-target training, while hAPP mice showed procedural learning deficits. In hidden-target learning and probe trials, hAPP mice and MCI-AD patients showed similar deficits in learning and remembering the target location. In addition, we have provided recommendations for selecting performance measures and sample sizes to make these assays sensitive to learning and memory deficits in humans with MCI-AD and in mouse models. Together, our results demonstrate that with careful study design and analysis, the Morris maze is a sensitive assay for detecting AD-relevant impairments across species.

    View details for DOI 10.1172/JCI78464

    View details for Web of Science ID 000370677300035

    View details for PubMedID 26784542

    View details for PubMedCentralID PMC4731157

  • Expression of A152T human tau causes age-dependent neuronal dysfunction and loss in transgenic mice. EMBO reports Maeda, S., Djukic, B., Taneja, P., Yu, G. Q., Lo, I., Davis, A., Craft, R., Guo, W., Wang, X., Kim, D., Ponnusamy, R., Gill, T. M., Masliah, E., Mucke, L. 2016; 17 (4): 530–51


    A152T-variant human tau (hTau-A152T) increases risk for tauopathies, including Alzheimer's disease. Comparing mice with regulatable expression of hTau-A152T or wild-type hTau (hTau-WT), we find age-dependent neuronal loss, cognitive impairments, and spontaneous nonconvulsive epileptiform activity primarily in hTau-A152T mice. However, overexpression of either hTau species enhances neuronal responses to electrical stimulation of synaptic inputs and to an epileptogenic chemical. hTau-A152T mice have higher hTau protein/mRNA ratios in brain, suggesting that A152T increases production or decreases clearance of hTau protein. Despite their functional abnormalities, aging hTau-A152T mice show no evidence for accumulation of insoluble tau aggregates, suggesting that their dysfunctions are caused by soluble tau. In human amyloid precursor protein (hAPP) transgenic mice, co-expression of hTau-A152T enhances risk of early death and epileptic activity, suggesting copathogenic interactions between hTau-A152T and amyloid-β peptides or other hAPP metabolites. Thus, the A152T substitution may augment risk for neurodegenerative diseases by increasing hTau protein levels, promoting network hyperexcitability, and synergizing with the adverse effects of other pathogenic factors.

    View details for DOI 10.15252/embr.201541438

    View details for PubMedID 26931567

    View details for PubMedCentralID PMC4818780

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