Bio

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

Contact

  • Academic
    cahayes3@stanford.edu
    University - Scholar Department: Epidemiology and Population Health Position: Postdoctoral Scholar

Additional Info

All Publications

  • Insulin-like growth factor-1 and cognitive health: Exploring cellular, preclinical, and clinical dimensions. Frontiers in neuroendocrinology Hayes, C. A., Wilson, D., De Leon, M. A., Mustapha, M. J., Morales, S., Odden, M. C., Ashpole, N. 2024: 101161

    Abstract

    Age and insulin-like growth factor-1 (IGF-1) have an inverse association with cognitive decline and dementia. IGF-1 is known to have important pleiotropic functions beginning in neurodevelopment and extending into adulthood such as neurogenesis. At the cellular level, IGF-1 has pleiotropic signaling mechanisms through the IGF-1 receptor on neurons and neuroglia to attenuate inflammation, promote myelination, maintain astrocytic functions for homeostatic balances, and neuronal synaptogenesis. In preclinical rodent models of aging and transgenic models of IGF-1, increased IGF-1 improves cognition in a variety of behavioral paradigms along with reducing IGF-1 via knockout models being able to induce cognitive impairment. At the clinical levels, most studies highlight that increased levels of IGF-1 are associated with better cognition. This review provides a comprehensive and up-to-date evaluation of the association between IGF-1 and cognition at the cellular signaling levels, preclinical, and clinical levels.

    View details for DOI 10.1016/j.yfrne.2024.101161

    View details for PubMedID 39536910

  • Empowering Early Career Researchers: The Jackson Heart Study Smith Scholars Program. Journal of racial and ethnic health disparities Hayes, C. A., Jones, R. 2024

    Abstract

    The University of Mississippi Medical Center Graduate Training and Education Center houses the Robert E. Smith, MD, Scholars Program, a two-year certificate program that equips predoctoral trainees from five Mississippi universities with advanced research skills in cardiovascular epidemiology. Funded by the National Heart, Lung, and Blood Institute (NHLBI), the program focuses on addressing health disparities, minority health, and health inequities in underserved communities. Trainees receive mentorship, career coaching, and a $7,500 annual stipend, building a foundation for postdoctoral opportunities and expanding professional networks. The Smith Scholars Program emphasizes population health and provides interdisciplinary training in areas such as biostatistics, scientific communication, and cardiovascular health. It is uniquely positioned to address systemic challenges, particularly in Mississippi, a state with high cardiovascular disease prevalence and limited research funding. The program's regional advantage and its partnership with the Jackson Heart Study offer scholars exposure to health disparities in Black/African American communities, preparing them to contribute to innovative, community-based research. Additionally, it fosters collaborative science, enabling participants to overcome academic barriers and engage with large-scale health equity research efforts. The Smith Scholars Program has been instrumental in shaping the career trajectories of its participants, facilitating their transition to postdoctoral positions and independent research roles.

    View details for DOI 10.1007/s40615-024-02226-3

    View details for PubMedID 39455520

  • Revolutionizing Postdoctoral Training Using the Social Ecological Model: Insights and Experiences from the Propel Scholars GEN BIOTECHNOLOGY Hayes, C. A., Headley, C. A., Nava, A. R., Vizcarra, E. A., Garcia, K. C., Mullen, M. S., Morales, J., Venida, A. C., Follis, S. 2024

    View details for DOI 10.1089/genbio.2024.0014

    View details for Web of Science ID 001283346900001

  • Unlocking the power of virtual networking for early-career researchers. eLife Hayes, C. A., Moore, J. T., Headley, C. A., Berrios-Negron, A. L., Lambert, W. M. 2024; 13

    Abstract

    Many successful researchers in the biomedical sciences have benefitted from mentors and networks earlier in their career. However, early-career researchers from minoritized and underrepresented groups do not have the same access to potential mentors and networks as many of their peers. In this article we describe how 'cold emails' and social media platforms - notably Twitter/X and LinkedIn - can be used to build virtual networks, and stress the need to invest in maintaining networks once they have been established.

    View details for DOI 10.7554/eLife.96381

    View details for PubMedID 38501601

  • 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

    Abstract

    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

https://orcid.org/0000-0002-6259-9456