J.D. Candidate at American University Washington College of Law
M.A. in Bioethics Candidate at New York University
M.S. in Cognitive and Information Sciences, University of California Merced
Researcher in Neuro-Computational Systems and Bioethics
I am a J.D. candidate at the Washington College of Law at American University, and researcher interested in the neuro-informational processes that give rise to and are instantiations of human time perception, active perception, and representation, and the biological mechanisms which underlie those processes in health and disease. I have two bachelor's degrees (a B.A. in Psychology and a B.A. in Philosophy) from San Francisco State University, and an M.S. in Cognitive and Information Sciences from the University of California, Merced, where I was principally advised by Dr. Noelle. I am in the process of defending my thesis for an M.A. in Bioethics at New York University, where I wrote on the importance of sentience in granting ethical consideration, the processes which underlie and instantiate brain death, and how these ought to inform our clinical and legal standards for declaring brain death, and on an ongoing project in Brooklyn, New York, where I am serving as the researcher responsible for developing and implementing a toxicological survey study.
The literature on Autism Spectrum Disorder (ASD) has come to characterize ASD as multifarious in both its etiology and its presentation. Here I disambiguate the structure underlying this heterogeneity by examining one genetic and two environmental precipitants of ASD, along bio-molecular and mechanistic lines. Along the way I also examine factors which influence the individual presentation of ASD attributable to those three precipitants, and outline three novel bio-molecular pathways which could help treat the causal mechanisms underlying ASD development and its treatment for those particular sub-types. I further describe and provide evidence for a causal mechanism which explains why Lithium administration reverses SHANK3 haploinsufficiency induced catatonia.
The visual system is often treated as a sequence of cortical stages, however, this approach does not straightforwardly predict or adequately explain perceptual aberrations such as blindsight and aphantasia. A mechanistic explanation of visual perception demands a model that captures how sensory representations become integrated into the broader perceptual apparatus. In this paper, I review the central white-matter and grey-matter networks and anatomy necessary to understand typical and atypical processing, and further present a systems-level framework unifying retinal and subcortical preprocessing, geniculostriate and tectopulvinar pathways, and a minimal cortico–basal ganglia–thalamic loop necessary for reportable perception. I characterize visual perception as a temporally extended process emerging from reciprocal interactions among anterior temporal semantic hubs, prefrontal evaluative systems, basal ganglia valuation circuitry, and thalamic global modulatory control. Using this architecture, I outline how perceptual phenomena like visual imagery arise from top-down propagations initiated in prefrontal cortex, routed through fronto-temporal fasciculi, and resolved as recurrently stabilized patterns in early visual cortex. I then examine how selective failures of pathway-specific integration generate distinct impairments: in blindsight, where preserved subcortical routes drive behavior without entering the global perceptual loop, and in aphantasia, where frontal and temporal representations cannot successfully entrain visual cortex despite intact conceptual structure. These cases demonstrate that access to visual information alone is insufficient for perceptual awareness; what matters is whether the information participates in the system-wide dynamics that constitute perception. This is important not only to discussion within cognitive science concerning the nature of visual perception, but may also serve the needs of clinicians and neurologists, by providing a framework potentially utile in allowing practitioners the ability to characterize lesions based on perceptual deficits. This framework provides a coherent computational and anatomical account of normal vision, imagery, and their dissociations. It also clarifies what these conditions imply, and do not imply, about the structure of perceptual experience, the functional role of feedback in the visual system, and the conditions under which neural activity becomes available to report.
Working Manuscript on the neuroscience and philosophy of brain death, how the law defines brain death, and the necessity for policy based on neurologically informed best practices.
An argument against time perception solely as either accumulatory or periodic within the mind. I argue there is a third option implied by a micro-circuit examination of time-telling in mouse striatum, rolling accumulatory window aggregation, which has been sparsely examined and which, in conjunction with the other modes of time-telling, answers some of the confounding questions relating to time perception on the scale of minutes to hours.
A selection of my academic presentations, including a talk and presentation on LSD proteomics at The University of Tokyo, a showcase speech on the computability of cognitive processes at St. Andrews University for the D.I. Summit, as well as talks on various subjects at less prestigious venues, like my talk on representational structures at Stanford University.
Miscellaneous experience, inside and outside of the academy, including experience as a teaching assistant at New York University for Medical Ethics, a research assistant at the Cognitive Computational Neuroscience Lab at UC Merced, and as the Membership Committee Chair at The American Psychological Association's 24th Division, the Society for Theoretical and Philosophical Psychology.
I have translated many smaller projects, and two versions of a book, 170 and 337 pages respectively, on the topic of STEAM education utilizing block code and arduinos, from Korean to English.