This study investigates how visual stimuli are processed by the human brain–specifically, faces. We hypothesize that facial recognition depends on a three-dimensional spatial framework. In order to test this, participants were given a 3D virtual reality headset in which faces were shown at different sizes but at a constant distance. Participants were shown three faces and asked to differentiate between them. In the first level, Scaling, faces were held at a constant distance while the size changed. The second level, Word No-Resize(WNR), consisted of the faces remaining the same absolute size but changing in depth, so the opening angle from the participants' perspective changed. The third level, Word Resize(WR), consisted of the faces again changing in depth but the faces were resized so that the opening angle remained constant at 8 degrees. Results show a V-shaped pattern in the reaction times for Scaling and WNR, however they remain constant for WR. Reaction times are lowest at an opening angle of eight degrees and increase as the size deviates from that, suggesting that faces are best processed at an eight-degree opening angle. The constant reaction times for WR show that depth does not have an effect on reaction time, while the opening angle does. As seen in the results of Scaling, reaction times differ even when the depth is constant as long as the size is changing, thus suggesting that depth perception for faces is dependent on size and not depth itself.

Early-emerging restricted and repetitive behaviors (RRBs) are a core feature of autism spectrum disorder (ASD) and may be predictive of later developmental outcomes. Understanding how these behaviors relate to broader domains of functioning and brain functional connectivity in infancy can inform early identification and intervention strategies. Here, we examine associations between RRBs and developmental outcomes at 12 and 24 months in infants at high and typical likelihoods for ASD. Next steps will relate RRBs to functional brain connectivity. Behavioral and fMRI data from the Infant Brain Imaging Study (IBIS), a longitudinal study of infants with high (HL) and typical (TL) familial likelihood for ASD were used in this study. RRBs were assessed at 12 and 24 months using the Repetitive Behavior Scale. Developmental outcomes were measured at 12 and 24 months using the Vineland-II, Mullen Scales of Early Learning, and Autism Observation Scale for Infants. In line with prior work, in HL infants, higher RRB scores at 12 months were significantly associated with lower adaptive functioning scores at 24 months (r = -0.37, p = 0.023). HL and TL groups also differed significantly across multiple domains, including cognitive, motor, language, and adaptive functioning. These findings suggest that early RRBs may serve as markers for later developmental challenges in infants at elevated likelihood for ASD. Future analyses will explore how RRBs relate to functional connectivity of the ventral tegmental area.

A major side effect of cisplatin, a widely used chemotherapy drug, is hearing loss and ototoxicity. There is extensive research on the effects of cisplatin on the cochlea, but not the vestibular system, particularly the afferent neurons of vestibular hair cells. This project examined the calyx, the dendrite of the vestibular afferent neuron, and its junction with the hair cell to observe if there were ototoxic effects on these structures that can serve as targets for otoprotectants. I hypothesized cisplatin would cause a partial collapse of the calyx, compromising the junction between the hair cell and calyx. I performed immunohistochemistry on the crista ampullaris of control and cisplatin treated mice, labeling the nuclei of hair cells and supporting cells, the cytoskeleton of the calyx, and a protein at the junction. In treated specimens, I observed no positive labeling for the calyx cytoskeleton or the protein at the junction, while nuclear labeling remained unchanged. These results suggest that cisplatin may damage the integrity of the calyx and the protein associating the hair cell to the calyx, or interfere with antibody binding sites. These findings reveal that cisplatin’s ototoxic effects go beyond the cochlea, deeming it necessary to investigate the vestibular system and its afferents to comprehensively understand its ototoxic effects and to develop effective treatments.

Clinical differences in Parkinson’s Disease (PD) is highly impacted by distinct patterns of tau aggregation in various neuropathologies. Tau is crucial to maintaining neuronal structural integrity and function. As a result, this protein is heavily implicated in neurodegenerative diseases, specifically when it is hyperphosphorylated and aggregates abnormally. In this sense, PD and other conditions that share this attribute are considered tauopathies. Previous studies have shown pathological tau aggregation to be a defining feature of tauopathies, but their accumulation and the inherent vulnerability of select brain regions present challenges to understanding PD progression. These aggregation patterns, known as tau strains, possess a myriad of conformations that may affect tau transmission and neurodegeneration, though these effects are not clearly understood. To investigate this, we developed advanced mouse models to identify tau strains and analyze their varying degrees of pathology. We will use bioimaging analysis software to illustrate different areas of the brain and annotate their local pathologies following the injection of pathological tau into diverse mice brain regions. By qualitatively observing these images and quantitatively classifying their neuropathological characteristics, we will be able to examine certain tau aggregates that will help us in predicting the progression of strain-specific tauopathies.

Jordan’s Syndrome (JS) is a rare neurodevelopmental disorder characterized by autism spectrum disorder (ASD) and macrocephaly, caused by de novo mutations in the PPP2R5D gene, which encodes a regulatory subunit of protein phosphatase 2A. PPP2R5D modulates the mTORC1 signaling pathway, which regulates the phosphorylation of proteins such as RPS6, influencing cell growth and proliferation. When dysregulated, PPP2R5D may enhance mTORC1 activity, leading to hyperphosphorylation of downstream effectors and possibly contributing to abnormal cell growth and macrocephaly. We hypothesized that PPP2R5D mutations result in hyperphosphorylation of RPS6 in neural progenitor cells (NPCs) derived from individuals with JS, compared to control NPC lines—an effect previously observed only in HEK293 cells. Western blot analysis confirmed line-dependent increases in phosphorylation of RPS6 in JS NPCs relative to controls. These findings support a disease mechanism involving overactivation of key growth signaling pathways in JS. They also suggest potential therapeutic avenues, such as targeting the mTORC1 pathway with pharmacological inhibitors to reduce hyperphosphorylation. Establishing baseline differences between JS and control NPCs provides a foundation for future experiments aimed at rescuing JS cellular phenotypes, such as assessing the therapeutic potential of the mTOR inhibitor rapamycin.