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You cannot spell without having a robust understanding of the alphabet; this sentiment also applies when evaluating functional circuitry without a complete knowledge of cell-to-cell communication strategies. My goal is to discern how variant groupings of cell signaling methods carry the piece-wise information underlying high-level cognitive output. When a circuit is compromised, so is the compounding information process. Compromised circuitry presents an opportunity to understand where the cell-to-cell communication failed in the context of the disease state that follows. In the Kozai lab, I utilize in-vivo two photon microscopy to investigate failure modes of neural interface implantation reported during human use. Neural interfaces are wonderful tools that both survey from and communicate with neuronal populations unless the brain variably reacts with what is called a foreign body response. This response differentially prevents neural interface efficacy by way of inflammation, glial cell activation, and peripheral immune cell recruitment. Interestingly, histological reports of responsive tissue post-implantation find proteins and cell morphologies common to Multiple Sclerosis, Alzheimer’s, Experimental Autoimmune Encephalomyelitis, and other neurodegenerative disorders. This means that the subcellular targets for probe-induced foreign body response may mirror the culprits of naturally occurring disease states. When optimizing neuronal interfaces for therapeutic strategies in Deep Brain Stimulation, Parkinson’s and Depression we can also broaden our understanding of context-dependent cell signaling events and connect our findings to histologically related disease states all while growing closer to understanding functional connectivity.

Prior to my time with Dr. Takashi Kozai, I worked with Dr. William Stauffer where I created a data acquisition program in Matlab to be used for optogenetic manipulations on rhesus macaques performing choice tasks. I was also responsible for the design, data collection, and processing of a decision-making study to further understand the cellular encoding of value-based reward. Before graduating with my B.S. in Neuroscience from the University of Pittsburgh, I worked in the labs of Dr. Howard Jay Aizenstein and Dr. Kenneth Fish. At the Aizenstein lab I processed structural and functional MRI data to study the effects of aging with a specific focus on white matter hyperintensities: pockets of ischemic white matter that appear very bright in MRI images. Experiments looked into the cognitive implications as white matter hyperintensities worsen from region-to-region. In Dr. Fish’s lab I explored whether GABAergic or glutamatergic signaling is altered in those with Schizophrenia. Utilizing stereological techniques, confocal microscopy and immunohistochemistry, I imaged layers 2 and 3 of rhesus monkey prefrontal cortex, a developmental comparison cohort used to determine the effect of age on synaptology. Along with the postmortem human tissue analysis, our team found that brain tissue from those with schizophrenia contained GABAergic interneurons with 18% fewer excitatory synapses.