Sarah was born and raised in Brazil where she attended law school before moving to the United States and shifting her interest to Neuroscience. She completed majors in Biology and Psychology at Virginia Commonwealth University (VCU) in 2020. At VCU, Sarah was part of the NIH-IMSD program and worked on uncovering mechanisms of axonal pathology in the lab of Dr. Jeff Dupree. She also worked on identifying the effects of income insecurity on decision-making in the lab of Dr. James Bjork. After graduating, Sarah worked at NIH as a UGSP Research Fellow and characterized a progranulin knockout mouse model in the lab of Dr. Alan Koretsky. She started her clinical work at NIH in the lab of Dr. Vijay Ramchandani where she worked to improve the diagnosis of alcohol use disorder. At Stanford, Sarah is interested in treating and managing neuropsychiatric disorders and increasing the representation of socially marginalized communities in research studies. When not in the lab Sarah enjoys reading, advocating for anti-poverty legislation, and hanging out with her son.

Education & Certifications

  • BS, Virginia Commonwealth University, Biology (2020)
  • BS, Virginia Commonwealth University, Psychology (2020)

Lab Affiliations

All Publications

  • Modifying the Emotion Regulation Brain Network in Depression: Mechanistic Insights From a Clinical Trial of Cognitive-Behavioral Therapy for Insomnia Krause, A., Izabel, S., Osorno, R., Solomon, N., Ahmadi, M., Lam, P., Magana, O., Blozyte, E., Cirelli, A., Harris, L., Bernert, R., Williams, L., Gross, J., Ma, J., Lazzeroni, L., Yesavage, J., Manber, R., Saletin, J., Goldstein-Piekarski, A. SPRINGERNATURE. 2023: 208-209
  • Schwann Cell Transplantation Subdues the Pro-Inflammatory Innate Immune Cell Response after Spinal Cord Injury INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Pearse, D. D., Bastidas, J., Izabel, S. S., Ghosh, M. 2018; 19 (9)


    The transplantation of Schwann cells (SCs) has been shown to provide tissue preservation and support axon growth and remyelination as well as improve functional recovery across a diverse range of experimental spinal cord injury (SCI) paradigms. The autologous use of SCs has progressed to Phase 1 SCI clinical trials in humans where their use has been shown to be both feasible and safe. The contribution of immune modulation to the protective and reparative actions of SCs within the injured spinal cord remains largely unknown. In the current investigation, the ability of SC transplants to alter the innate immune response after contusive SCI in the rat was examined. SCs were intraspinally transplanted into the lesion site at 1 week following a thoracic (T8) contusive SCI. Multicolor flow cytometry and immunohistochemical analysis of specific phenotypic markers of pro- and anti-inflammatory microglia and macrophages as well as cytokines at 1 week after SC transplantation was employed. The introduction of SCs significantly attenuated the numbers of cluster of differentiation molecule 11B (CD11b)⁺, cluster of differentiation molecule 68 (CD68)⁺, and ionized calcium-binding adapter molecule 1 (Iba1)⁺ immune cells within the lesion implant site, particularly those immunoreactive for the pro-inflammatory marker, inducible nitric oxide synthase (iNOS). Whereas numbers of anti-inflammatory CD68⁺ Arginase-1 (Arg1⁺) iNOS- cells were not altered by SC transplantation, CD68⁺ cells of an intermediate, Arg1⁺ iNOS⁺ phenotype were increased by the introduction of SCs into the injured spinal cord. The morphology of Iba1⁺ immune cells was also markedly altered in the SC implant, being elongated and in alignment with SCs and in-growing axons versus their amoeboid form after SCI alone. Examination of pro-inflammatory cytokines, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and anti-inflammatory cytokines, interleukin-4 (IL-4) and interleukin-10 (IL-10), by multicolor flow cytometry analysis showed that their production in CD11b⁺ cells was unaltered by SC transplantation at 1 week post-transplantation. The ability of SCs to subdue the pro-inflammatory iNOS⁺ microglia and macrophage phenotype after intraspinal transplantation may provide an important contribution to the neuroprotective effects of SCs within the sub-acute SCI setting.

    View details for DOI 10.3390/ijms19092550

    View details for Web of Science ID 000449988100086

    View details for PubMedID 30154346

    View details for PubMedCentralID PMC6163303

  • Dendrite regeneration of adult Drosophila sensory neurons diminishes with aging and is inhibited by epidermal-derived matrix metalloproteinase 2 GENES & DEVELOPMENT DeVault, L., Li, T., Izabel, S., Thompson-Peer, K. L., Jan, L., Jan, Y. 2018; 32 (5-6): 402-414


    Dendrites possess distinct structural and functional properties that enable neurons to receive information from the environment as well as other neurons. Despite their key role in neuronal function, current understanding of the ability of neurons to regenerate dendrites is lacking. This study characterizes the structural and functional capacity for dendrite regeneration in vivo in adult animals and examines the effect of neuronal maturation on dendrite regeneration. We focused on the class IV dendritic arborization (c4da) neuron of the Drosophila sensory system, which has a dendritic arbor that undergoes dramatic remodeling during the first 3 d of adult life and then maintains a relatively stable morphology thereafter. Using a laser severing paradigm, we monitored regeneration after acute and spatially restricted injury. We found that the capacity for regeneration was present in adult neurons but diminished as the animal aged. Regenerated dendrites recovered receptive function. Furthermore, we found that the regenerated dendrites show preferential alignment with the extracellular matrix (ECM). Finally, inhibition of ECM degradation by inhibition of matrix metalloproteinase 2 (Mmp2) to preserve the extracellular environment characteristics of young adults led to increased dendrite regeneration. These results demonstrate that dendrites retain regenerative potential throughout adulthood and that regenerative capacity decreases with aging.

    View details for DOI 10.1101/gad.308270.117

    View details for Web of Science ID 000428519800009

    View details for PubMedID 29563183

    View details for PubMedCentralID PMC5900713