Cellas is currently a postdoctoral fellow/Propel scholar at Stanford University in the Department of Neurology and Neurological Sciences in a laboratory utilizing longitudinal data analysis and neuroimaging modalities to understand the aging brain, neuropathology, cognition, and Alzheimer’s Disease. Postdoctoral experience includes using R, Linux, and Python to perform data preprocessing, multivariate statistical analysis, and applying novel models for longitudinal continuous outcomes. Cellas received his Bachelor’s in Biology (2015-2019) and Doctor of Philosophy in Pharmaceutical Sciences with an emphasis in Pharmacology (2019-2022) from the University of Mississippi. As a doctoral candidate, his research focused on using both in vitro and in vivo approaches to further elucidate how neuroendocrine modulation specifically insulin-like growth factor-1 alters learning and memory performance along with ischemic stroke outcomes. Skills gained during doctoral training included in vitro cell culture, pharmacological experimental design of both in vitro and in vivo studies, development of transgenic mouse models, a wide array of rodent behavioral paradigms, stereotaxic surgery, photothrombosis, and numerous ex vivo cellular, molecular, and microscopy techniques.
My primary interests lie at the intersection of aging, neurodegenerative disease, and using longitudinal epidemiological data sets to investigate hypotheses. All around neuroscientist seeking sci-comm, industry, and academic opportunities to strengthen skills to become an independent investigator.

Stanford Advisors

All Publications

  • Academic ethics of mental health: the national black postdocs framework for the addressment of support for undergraduate and graduate trainees. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology Hayes, C. A., Berrios-Negron, A. L., Tamir, T., Hardeman, K. N., Heyward, F. D. 2024

    View details for DOI 10.1038/s41386-023-01787-x

    View details for PubMedID 38191654

    View details for PubMedCentralID 7199285

  • Neuronal and Astrocyte Insulin-like Growth Factor-1 Signaling Differentially Modulates Ischemic Stroke Damage. bioRxiv : the preprint server for biology Hayes, C. A., Morgan, N. I., Thomas, K. C., Pushie, M. J., Vijayasankar, A., Ashmore, B. G., Wontor, K., De Leon, M. A., Ashpole, N. M. 2023


    Ischemic stroke is a leading cause of death and disability, as therapeutic options for mitigating the long-term deficits precipitated by the event remain limited. Acute administration of the neuroendocrine modulator insulin-like growth factor-1 (IGF-1) attenuates ischemic stroke damage in preclinical models, and clinical studies suggest IGF-1 can reduce the risk of stroke and improve overall outcomes. The cellular mechanism by which IGF-1 exerts this protection is poorly defined, as all cells within the neurovascular unit express the IGF-1 receptor. We hypothesize that the functional regulation of both neurons and astrocytes by IGF-1 is critical in minimizing damage in ischemic stroke. To test this, we utilized inducible astrocyte-specific or neuron-specific transgenic mouse models to selectively reduce IGF-1R in the adult mouse brain prior to photothrombotic stroke. Acute changes in blood brain barrier permeability, microglial activation, systemic inflammation, and biochemical composition of the brain were assessed 3 hours following photothrombosis, and significant protection was observed in mice deficient in neuronal and astrocytic IGF-1R. When the extent of tissue damage and sensorimotor dysfunction was assessed for 3 days following stroke, only the neurological deficit score continued to show improvements, and the extent of improvement was enhanced with additional IGF-1 supplementation. Overall, results indicate that neuronal and astrocytic IGF-1 signaling influences stroke damage but IGF-1 signaling within these individual cell types is not required for minimizing tissue damage or behavioral outcome.

    View details for DOI 10.1101/2023.04.02.535245

    View details for PubMedID 37034764