The human brain can internally represent three-dimensional (3D) spatial information from external visual input despite its retina receiving photo signals in two-dimensional (2D) form. However, it is not completely understood how the brain can compute 3D space from 2D information. According to principles of cortical magnification, the center of human vision from the fovea is in great detail, with less detail in the periphery. Consequently, the mapping from the retina is roughly log-polar in the primary visual cortex, as significantly more neurons are dedicated to processing the visual information from the fovea. We hypothesized that reaction times to stimuli presented to be based on the absolute distance away from our focused center of vision and should increase proportional to log-distance. In our experiment, participants were shown one of three letters (E, B, P) using a virtual reality headset and instructed to press the corresponding key (V, B, N) assigned to each letter on a keyboard. The three letters were projected randomly at an intersection within a 7-by-7 grid on the screen of the VR headset, ranging from -24° to 24° horizontally and vertically, in 8° intervals. Statistical analysis revealed that reaction time is correlated with the absolute distance from the center of focused vision, supporting the hypothesis of the log-polar coordinate system.

Parkinson’s Disease is a neurodegenerative disorder characterized by motor dysfunction including tremor, stiffness, and freezing of gait. Tremor, one of the most well-known Parkinson’s symptoms, is caused by dysregulation of the motor circuit. The basal ganglia, specifically the subthalamic nucleus (STN), is a key component of this circuit, and plays a role in regulating voluntary motion and suppressing unwanted/excessive motion. My hypothesis is that there is a correlation between Parkinson’s tremor severity and functional connectivity of the STN. This investigation used motor evaluations and resting-state fMRI data from a clinical study of Parkinson’s patients. Tremor severity was analyzed and quantified from patients’ motor evaluations, and fMRI data was preprocessed using FSL tools fmriprep and fsl fix. Preprocessing included image extraction, registration to standard space, and alignment. A seed-based analysis will be conducted to determine STN functional connectivity and examine its correlation to symptom severity. Parkinson’s is the most common movement disorder in the United States, and its pathology and treatment are still not well-understood. This research fills a gap in current literature, as there are few studies investigating the correlation between STN connectivity and tremor, particularly using seed-based methods. Therefore, this study will provide insight into structural and functional changes associated with Parkinson’s tremor, contributing to vital knowledge regarding diagnosis and treatment of the disease.

In previous studies, a high correlation has been shown between Alzheimer’s Disease and seizure activity. More specifically, hyperexcitability has been shown to speed up the progression of Alzheimer’s Disease (AD). One mouse model for AD is the J20 model, which has naturally decreased levels of KV 1.1 receptors. Low levels of KV 1.1 receptors results in hyperexcitability, which has been measured using SPIKE scoring. In this project, multiple crosses of mice lines were conducted to determine if protein expression of KV 1.1 can be rescued with the BAC gene in J20 mice. The larger picture of this study is if there is a possibility that KV 1.1 rescue with the BAC gene can decrease the progression of AD. In order to answer the question, three cross of mice have been conducted (J20/WT, J20 * KV 1.1 BAC, and J20/KVBAC) in addition to having wild type mice as controls. Perfusion of the mice was performed, followed by brain collection and microdissection in order to obtain somatosensory and hippocampal tissue of each sample. Following somatosensory tissue collection, Western blots were performed to determine if KV 1.1 protein expression could be rescued in mice with BAC gene. To test if rescue of KV 1.1 with BAC decreased hyperexcitability of the J20 mice, SPIKE scoring was conducted for all mouse models and compared. Increases in SPIKEs were also correlated to REM sleep stages.

Traumatic brain injury (TBI) results from biomechanical forces impacting the brain and may lead to post-traumatic epilepsy (PTE). Although numerous antiepileptic drugs exist, they have not proven effective in reversing or preventing PTE. This study investigated Levetiracetam’s (LEV) effects on seizure development following severe TBI. Adult male Sprague-Dawley rats (300-350 g at the time of TBI) underwent a left lateral fluid percussion injury (LFPI). After LFPI, LEV-treated rats (LEV; n=x) received 200 mg/kg bolus injection i.p. followed by 200 mg/kg/day via an s.c. minipump for 3 months. Vehicle-treated rats (VEH; n=) underwent the same procedures, except LEV was replaced with PBS 1%. Immediately after FPI induction, all the animals were implanted with bilateral frontal, central, and occipital screws and 2 paired perilesional cortical and hippocampal microelectrodes. EEG activity was recorded for 2 weeks post-injury, then monthly until week 28–29 (month 7), when final evaluations were conducted. We compared seizure frequency, duration, and electrographic features between groups to assess whether early LEV administration alters seizure progression or severity over time. Preliminary findings suggest that LEV treatment during the acute phase may reduce early seizure burden and modulate long-term epileptiform activity. These results offer insights into the temporal dynamics of seizure development after TBI and support the potential of early pharmacological intervention in mitigating PTE risk.

Huntington’s Disease (HD) is a fatal late-onset neurodegenerative disorder that follows an autosomal dominant inheritance pattern. It manifests with progressive chorea, cognitive decline leading to dementia, and psychiatric disturbances. HD is caused by a CAG repeat expansion in the huntingtin (HTT) gene corresponding to an expanded polyglutamine tract in the mutant huntingtin (mHTT) protein. While wild-type HTT is exported to the cytoplasm, mHTT accumulates in the nucleus, where it can form aggregates or toxic oligomers. Recent studies have implicated mHTT in the disruption of nuclear processes, including DNA mismatch repair. However, its role in impairing transcriptional regulation remains less understood. Our previous proteomic analyses identified differential expression of key transcriptional regulators RNA Polymerase II (Pol II) and Topoisomerase I (Top1). In this study, we compared the expression patterns of Pol II and Top1 across four genotypes, including wild-type mice and an HD mouse model expressing the human mHTT gene. Immunohistochemistry of striatal tissue revealed that both Pol II and Top1 undergo physical changes in HD-affected cells. Pol II exhibits nuclear phase separation, shifting from diffuse to punctate expression patterns, while Top1 shows increased colocalization with chromatin foci, which intensifies with age. These findings suggest possible interactions between mHTT and key transcriptional regulators and offers insight into mHTT’s role in HD pathogenesis by disrupting transcription.