Robert B. Glassman Memorial Brain, Mind, and Behavior Symposium

October 31 — Undergraduate and Alumni Research Poster Session

View the poster abstracts

4:00 - 6:30 p.m., Calvin Durand Hall, Mohr Student Center

4:00 p.m. Chicago Society for Neuroscience Reception

4:30 p.m. Welcome Remarks and Unveiling of Annual Neuroscience Sculpture

4:45 - 6:10 p.m. Poster Viewing
Enjoy posters and exhibits by current students and recent alumni of original student/faculty research conducted at Lake Forest, Rosalind Franklin University of Medicine and Science, and several other Chicago area research universities and beyond. 

6:10 p.m. Closing Ceremony
Introduction, Nu Rho Psi
Closing Remarks for Brain Awareness Week and Glassman Symposium
Recognition of student scholars and celebratory photo

2025 Student and Alumni Poster Abstracts

Alumni abstracts

Functional Integration Of Small Cell Lung Cancer Drives Synaptic Remodeling Of Neurons

Aiden J. Houcek ’20^1,2,3, Burak Uzay^1,2, Geena Ildefonso⁴†, Tolu Omokehinde⁴†, Lisa M. Monteggia^1,2, Vito Quaranta^1,4, Amanda Linkous¹, Ege T. Kavalali^1,2*

¹Department of Pharmacology, Vanderbilt University; Nashville, TN, USA
²Vanderbilt Brain Institute, Vanderbilt University; Nashville, TN, USA
³Department of Biological Sciences, Vanderbilt University, Nashville, TN, USA
⁴Department of Biochemistry, Vanderbilt University, Nashville, TN, USA
*Corresponding author. Email: ege.kavalali@vanderbilt.edu
† These authors contributed equally to this work

Tumor cell plasticity in novel microenvironments is central to the integration and subsequent growth of metastatic cells. However, the functional consequences of tumor cell integration with central neurons remains understudied. Here, we address this question using small cell lung cancer (SCLC), which has an extraordinary propensity to metastasize to the brain in humans. Electrophysiological analysis of SCLC cells in neuronal microenvironments reveal functional synapse formation between neurons and a subset adjacent SCLC cells. This synaptic integration of SCLC into neuronal microenvironments induced multiplicative synaptic scaling and altered neuronal excitability between surrounding induced human neurons. Aberrant excitation in human neurons with SCLC was sustained by synaptic NMDA receptor activation and can be reduced by the FDA approved NMDA receptor blocker memantine. These findings reveal strategies to normalize tumor-induced exacerbation of aberrant neuronal activity.

Contribution of the anterior cortical amygdala to adolescent and adult rat social interaction

Rose J. Montes ’24 and Nicole C. Ferrara, Center for Neurobiology of Stress Resilience and Psychiatric Disorders, Rosalind Franklin University of Medicine and Science, IL, 60064, USA

Adolescent development is a critical period for the acquisition of social skills and exploratory behaviors that coincides with neural maturation. As such, adolescents are especially sociable, and as a consequence, have a heightened sensitivity to social disruptions. Social deprivation, in particular, limits the adolescent social repertoire and in doing so can drive a number of social behaviors. This adolescent sensitivity to social deprivation is believed to be a result of ongoing functional changes in the amygdala.  Despite the evidence showing it receives dense inputs from areas that play key roles in exploratory and social behaviors, very little is known about the anterior cortical amygdaloid nucleus (ACo) subregion, especially during development. Our study was designed to first quantify developmental differences in ACo activity and then understand how social deprivation shapes ACo-mediated open field exploration and social behavior in adolescents and adults.  Consistent with previous literature, we found that younger age groups socially interact more than adults. In those younger groups, we found higher levels of cellular activity  in the ACo when compared to adult rats using an immunofluorescent approach. However, ACo activity negatively correlated with the degree of social interaction, suggesting that ACo activity is heightened in younger relative to adult age groups but this activity decreases with greater degree of social interaction.  Similarly, we found that adolescent ACo neuronal firing was higher than adults, and ACo neuronal firing was reduced following social deprivation. This effect was especially pronounced in adolescents. Based on our data, we next used a chemogenetic approach to inhibit the ACo in combination with social deprivation to test the hypotheses that 1) the adolescent and adult ACo would regulate exploration and social behaviors but this would be more pronounced in adolescents, and 2) ACo inhibition would be blunted with social deprivation. Adolescent ACo inhibition had little effect on social behavior, while adult ACo inhibition selectively increased social play. Following social deprivation, adolescents increased overall social interaction and play while ACo inhibition modestly reduced social play. Social deprivation had little effect on adult behavior. These findings highlight an important role for the ACo in social play with age that may be reshaped following social deprivation to change the necessity of the ACo to social behaviors. Together, our work identifies novel developmental differences in ACo activation and suggests that social deprivation alters the necessity of the mature ACo for exploratory and social behaviors.

paRsynth: An open-source computational tool to Sonify Character Strings for Bioacoustics Research

Raneem Samman ’24^1,2, Alexandra G. Juarez¹, Grace Smith-Vidaurre^1,2,3.

¹Department of Integrative Biology, Michigan State University, East Lansing, MI, USA
²Department of Computational Mathematics, Science, and Engineering, Michigan State University, East Lansing, MI, USA
³Ecology, Evolution, and Behavior Program, Michigan State University, East Lansing, MI, USA 

Quantitative analyses of animal sounds are critical to address why and how communication systems evolved, including systems that rely on social learning. Longstanding hypotheses propose that the production of socially learned vocalizations in distantly related mammals and birds, including humans, originated to communicate information about social identity, such as group and individual identity. Testing these ideas can give us insights into the evolutionary origins of the social learning of vocalizations, or vocal learning. However, empirical datasets are often noisy and incomplete, and the identity information encoded in these vocalizations is unknown, making it difficult to test theoretical predictions. To address this challenge, we developed an open-source R package, paRsynth, for creating synthetic vocalizations with controlled identity information encoding in the shape of vocalizations, or frequency modulation patterns. The package enables users to customise synthetic vocal signals by combining group identity, individual identity, and random variation components in character strings that are sonified into audio files. In addition, we developed a second version of this package that facilitates greater flexibility of information encoding, including manipulating the location of identity information along character strings. By offering a flexible pipeline for the generation of synthetic vocalizations with different types and amounts of identity information, paRsynth is a valuable tool for future simulation-based research on how information encoding may have been important for the evolution of vocal learning.

State Parental Consent Law and Treatment Use Among Adolescents With Depression

Jessica Lee Schleider ¹, Amanda Smock ¹, Isaac Lev Ahuvia ², Tubanji Walubita ’19 ¹, Andy Seth Rapoport ¹, Shannon Hill ¹, Jonathan Purtle ³

¹Department of Medical Social Sciences, Northwestern University Feinberg School of Medicine, Chicago, Illinois
²Department of Psychology, Stony Brook University, Stony Brook, New York
³Department of Public Health Policy and Management, New York University School of Global Public Health, New York

Depression is a leading public health concern among U.S. adolescents, yet many do not receive treatment. A potential barrier is state parental consent laws, which vary across states and may restrict adolescents’ ability to access care independently. This study examined the association between state consent laws and treatment access among adolescents with depression. We conducted a legal mapping study using LexisNexis and Justia Law to systematically identify and code laws in all 50 states and Washington, D.C., regarding adolescents’ ability to independently consent to mental health services. Laws were classified into two categories: (1) parental consent always required and (2) independent minor consent sometimes or always allowed. These legal classifications were linked to state-level data from the 2021-2022 National Survey on Drug Use and Health (NSDUH), which estimates the percentage of adolescents (ages 12-17) with a past-year major depressive episode (MDE) who received treatment. Analysis of covariance tested whether treatment use differed by state consent laws, adjusting for state-level prevalence of adolescent depression. In states that always require parental consent, 37.2% of adolescents with MDEs accessed treatment, compared to 46.7% in states that allowed adolescent consent with no or limited restrictions. This nearly 10-percentage-point difference was statistically significant (F_1,46 = 11.18; P = .002; η²p = .21). These findings highlight how state laws can directly influence access to care during a critical developmental period.

Prioritizing Clinical Utility In The Association Between Allostatic Load And The Consequences Of Stress

Walts ZL ‘21*, Cochran A, Zinfandel M, Trentham Deitz A, Owusu-Brackatt N, Rosenkranz M, Ersig A, Shrubsole M, Warren Andersen S. Department of Population Health Science, University of Wisconsin Madison, Madison, WI 53706

Student abstracts

Investigating IGFBP-1 & IGF-1 Levels in Serum to Evaluate Women with Recurrent Reproductive Failures

Amy Adamik ‘26, and Mahmood Bilal, Riyas AliAp, Joanne Kwak-Kim, Svetlana Dambaeva, Clinical Immunology Lab, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064

Recurrent reproductive failure, like recurrent pregnancy loss (RPL) and recurrent implantation failure (RIF), impacts millions of women globally and an estimated 15% of women of childbearing age in the United States, with ovulatory disorders identified as a primary contributing factor. Current diagnosis for these conditions relies on patient history and invasive procedures such as endometrial biopsy, as no reliable serum tests exist to identify women at risk for reproductive failure. One promising marker for serum testing is insulin-like growth factor binding protein-1 (IGFBP-1), a key regulator of insulin-like growth factor-1 (IGF-1) abundance, a growth factor that is known to affect endometrial receptivity and placental development. The primary goal of this project was to validate a human-specific IGFBP-1 immunoassay (ELISA) for use in patient serum testing. Initial testing found that the manufacturer’s standard curve produced reliable values only in the proposed analytical mid-range, while high and low concentrations were inconsistent. To address this, we developed a modified standard curve that improved linearity and reduced variability. Utilizing this modified assay, we compared serum levels of IGFBP-1 and IGF-1 in patients with RPL or RIF. Preliminary findings saw a non-significant difference of IGFBP-1 and IGF-1 serum levels between RIF and RPL patients. Unexpectedly, we saw no significant correlation between IGFBP-1 and IGF-1 serum levels. These findings could reflect the role of IGFBP-3, which binds 80% of circulating IGFs and could reduce detectable free IGF-1 in serum. Future studies will focus on sample testing, which we expect to find significance with a larger sample size.

Region-Specific Role of Microglial C3aR1 in Neural Inflammation in Obesity

Martha S. Alatorre Martínez ’26, Jean-Pierre Pallais, Maria Razzoli, Alessandro Bartolomucci, Department of Integrative Biology and Physiology, University of Minnesota Medical School, Jackson Hall 6-125 321 Church St. SE Minneapolis, MN 55455

Obesity is a chronic inflammatory condition that not only affects metabolism but also increases the risk for cognitive decline and neurodegenerative diseases. One way this happens is through neuroinflammation, especially in areas like the hypothalamus. This process is driven by glial cells like microglia and astrocytes both of which play a role in innate immunity. Glial cells have been shown to be upregulated in obesity and may contribute to this brain inflammation. In the brain, the Complement 3a Receptor 1 (C3aR1) is only expressed in microglia and has been linked to inflammation and neurodegenerative processes. We aim to investigate whether microglial C3aR1 plays a role in diet-induced neuroinflammation. To do this, we used a tamoxifen-inducible mouse model to knock out C3aR1 in microglia and then exposed animals to either a high-fat diet (HFD) or standard diet (SD) for either 12 or 32 weeks. Using immunofluorescence, we looked at markers of gliosis in different brain regions including the hypothalamus, cortex, and hippocampus. We found that HFD increased gliosis mainly in the hypothalamus, while the cortex and hippocampus showed less consistent changes in spite of prolonged exposure to the high fat diet conditions. Additionally, knocking out C3aR1 in microglia reduced hypothalamic gliosis in HFD animals.These results suggest that microglial C3aR1 is involved in the brain’s inflammatory response to diet and might play a crucial role in obesity related neuroinflammation.

Characterizing sniffing behavior in head-fixed mice

Marcelo A. Camba Almazan ’26, Youjin Lee, EunJung Hwang, Kaiwen Kam, Dept. of Cell Biology and Anatomy, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60044

Breathing is necessary to sustain life. Breathing seems simple, but it must adapt to our body’s responses to the environment and coordinate with other behaviors such as speech. The preBötzinger complex (preBötC), a brainstem nucleus in the ventrolateral medulla, is critical for generating respiratory rhythm. Beyond breathing at rest, preBötC also generates other breathing-related rhythms, such as sighing and sniffing. How preBötC generates these multiple rhythms is not known. Sniffing in mice is a fast respiratory rhythm that we hypothesize is dependent on an ionic current, known as the hyperpolarization-activated current (I_h) in the preBötC. The goal of this research project was to characterize sniffing behavior after blockade of I_h in awake, head-fixed mice. Breathing and sniffing were measured using a thermistor placed in front of the nose to detect temperature changes associated with airflow. We used custom procedures written for Igor Pro to analyze the thermistor recording by detecting the peaks (difference between inhaled and exhaled air temperature) in order to detect the rate of exhalations per session. We found that breathing and sniffing were highly variable in awake mice and did not detect consistent changes due to I_h blocker injection. We conclude that alterations in the experimental protocol may be necessary to reduce variability and observe changes in breathing and sniffing due to the pharmacological blockade of I_h.

Quantification of AD Pathology in the Cortex of a 3xTG Mouse Model

Lia Alterson ’27, Nikki Barrington, and Beth Stutzmann, Center for Neurodegenerative Disease and Therapeutics, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60045

Alzheimer’s Disease (AD) is commonly characterized by cognitive and behavioral deficits that progress with age. The unique pathology of this disease includes the aggregation of amyloid beta plaques, as well as tangles of hyperphosphorylated neurofibrillary tau proteins. Microglia, the brain's immune response cells, are also dysfunctional in Alzheimer’s disease. To model this disease, the 3xTg-AD transgenic mouse model expressing human presenilin-1 protein (PS1), amyloid precursor protein (APP), and tau protein is often used, as amyloid beta plaques and neurofibrillary tangles progress in a similar manner to humans. In this study, we aimed to investigate how the concentration of these neuropathological hallmarks of AD change in the cortex with age. Specifically, we hypothesized that cortical concentrations of amyloid beta plaques, hyperphosphorylated neurofibrillary tau proteins, and microglial cells would increase with age. Using immunohistochemistry in the 3xTg-AD mouse model, we were able to quantify and compare cortical amyloid beta plaques, phosphorylated tau proteins, and microglial cells between 6–8-month-old, 9–11-month-old, and 12+ month old groups. We found a significant increase in the concentration of cortical amyloid beta plaques with increasing age. We also found that cortical concentrations of phosphorylated tau protein significantly increased with age, specifically between the 6–8-month-old and 9–11-month-old groups. We did not find a significant difference in cortical microglia concentration between age groups. Collectively, these findings provide insight into the pathological progression of Alzheimer’s disease in a 3xTg

mouse model, which is important for efforts aiming to combat this disease.

Examining Cognitive and Noncognitive Factors Predicting Student Achievement in a Low-Income Middle School: Future Directions for Intervention at the Student and Teacher Level

Jackson Rothman ’25, Ena Sehic ’26, Margaret Fields ’26, Nicole Golden ’25, Valeriya Mamatkazina ’27, Ava Jarock ‘27

Project Advisors: Elayne Vollman and Dawn Abt-Perkins

Inequality in learning opportunities is one of the most fundamental problems facing education in the US. Suffering most, especially following the COVID-19 crisis, are low income, minority communities (Francis et al., 2022). Place-based research strategies which effectively address complex problems (Schapke et al., 2022) have implications for student engagement and community improvement. This research utilizes a research-practice partnership with a middle school of primarily low-income, immigrant children from Mexico and Central America. To better understand the chosen school’s low graduation rates and achievement outcomes, we examined the landscape of cognitive and noncognitive factors such as growth mindset, sense of belonging, math anxiety, and mind wandering, as well teacher beliefs and practices and how these factors can influence student’s mathematics achievement. Analyses revealed that student cognitive and noncognitive factors are significant predictors of mathematics achievement. A discrepancy in the teacher's mindset and student's mindset was also found. To address this discrepancy and the low achievement in the chosen school, our current work is implementing a concurrent teacher and student mindset intervention to examine whether simultaneous intervention at multiple levels can produce compounding positive effects for student mindset and achievement. In partnership with David Yeager at the University of Texas at Austin, this “values-aligned” intervention encourages teachers to adopt a growth mindset view of their students by aligning those practices with their core professional values. Students in our study will be randomly assigned to either the mindset intervention or a control intervention which teaches cognitive strategies for learning. This novel methodology has not been utilized with these intervention measures (Hecht et al., 2023) and will allow us to test this double-dose effect. This poster will outline key components of the interventions and the proposed research plan with study goals to bridge the gap in the literature on whether student growth mindset interventions can be better supported by effective teacher interventions.

Arm-Based Haptic Feedback Enables Intuitive Object Perception in Absence of Vision

Paul Benjamin ‘28, Frederick R Prete, Biology Department, Lake Forest College, Lake Forest, IL 60045

Approximately 8.6 million North Americans are blind or low vision (B/LV), and 1.5-2.0 million rely on mobility aids. Haptic vibrations, which stimulate somatosensory receptors, are widely used in consumer devices and can indicate object proximity. We explored implementing haptic stimuli in a hands-free, arm-mounted assistive device using an MB1040 LV-MaxSonar-EZ4 distance sensor (20Hz) and a Precision Microdrive ERM vibrating motor driven by a DRV2605 chip. In Experiment 1, subjects (N=14) reported perceived distance of a 12”x16” card at upper-arm height, placed randomly at five distances (<1, 1-2, 2-3, 3-4, and >4 ft) to their left or right. Each distance was assigned a predetermined haptic stimulus intensity that negatively correlated with object distance (100%, 82%, 65%, 35%, and null, respectively). Pre- and post-tests, separated by an unsupervised familiarization period in which subjects were allowed to walk around wearing the mobility device, did not differ. Users’ distance perceptions were strongly correlated with stimulus intensity (R² = 0.977, n = 5, p < 0.001), indicating reliable discrimination of object proximity based on haptic intensity. In Experiment 2, we integrated an Inertial Measurement Unit (IMU) LIS3DH accelerometer to the mobility aid to constrain feedback when the subject is stationary. Velocity values across five 1-minute trials under two conditions (Stationary vs. Moving) indicated haptic feedback could be restricted during movement at less than 14 steps per minute, limiting output in realistic mobility conditions. These findings support upper-arm vibrational feedback as a viable strategy for object perception in low-vision users.

Insight into Synucleinopathies in a Yeast Model: Unravelling Molecular Determinants of β−Synuclein and γ-Synuclein Toxicity

Leslie Casares ‘26, Holly Kiernan ‘26,  Shanamon Chandavimol ‘27, Federica Bertolotti ‘24, Sebastian Gacek ‘25, Shubhik DebBurman, Neuroscience Department and Biochemistry & Molecular Biology Program, Lake Forest College, Lake Forest, Illinois 60045

Synucleinopathies, a group of disorders characterized by the abnormal folding and aggregation of proteins from the synuclein family (including α-, β-, and 𝛾-synuclein), includes Parkinson’s Disease (PD), the second most prevalent neurodegenerative condition. While α-synuclein's role in PD is well established, less is understood about the involvement of β- and 𝛾-synucleins in neurodegeneration and toxicity. However, two mutations in β-synuclein (P123H and V70M) are associated with Dementia with Lewy Bodies (DLB). In our Saccharomyces cerevisiae (budding yeast) PD model system, we recently discovered that β-synuclein is toxic but less than α-synuclein and 𝛾-synuclein is non-toxic. Here, we further expanded our evaluation of the toxicity potential of β- and 𝛾-synuclein. 1) To understand whether familial mutant toxicity was due to loss of the original amino acid or gain of the new mutant, we evaluated substitution mutants for V70M and P123H by changing the original amino acid with representative polar, nonpolar, basic, and acidic residues. For the V70 position, we found that the level of hydrophobicity was key for toxicity and aggregation. For the P123 position, we observed more evidence for the loss of the original proline than for the gain of the mutant basic amino acid. 2) We swapped the known familial mutations in α- and β-synuclein onto other synucleins at conserved locations. We found that α-synuclein familial mutations linked with amino acids A18, A29, A30, E46, G51, and A53 can differentially regulate β-synuclein toxicity, however, 𝛾-synuclein’s non-toxicity remains unaltered with α-/β- familial swap mutations at A18, A30, E46, and V70. 3) We combined both V70M and P123H mutants and found their combinatorial toxicity to be additive. 4) We assessed the impact of altering those amino acids in β- and 𝛾-synucleins which are conserved post-translational modification sites from α-synuclein. We found that putative acetylation (K6), nitration (Y39), SUMOylation (K85) and phosphorylation (S118) sites in β-synuclein regulate its toxicity. In γ-synuclein, only putative acetylation site (K6) regulates its toxicity. 5) We also found that several synucleinopathy-linked environments modelled in genetically altered yeast strains can increase both β- and 𝛾-synuclein toxicity. 6) Finally, we used AlphaFold to generate predicted protein models for all three synucleins, which show that β-synuclein can polymerize like α-synuclein (but requires at least seven monomer additions), while γ-synuclein never aggregates. This study highlights the usefulness of yeast and AI models in better understanding β- and γ-synuclein pathogenicity in neurodegeneration.

New Molecular Insights into the Toxicity Linked with Three Newer α-Synuclein Mutants (A18T, A29S, and A53V) in a Yeast Model

Shanamon Chandavimol ‘27, Kate Feist ‘27, Sharbanu Elmi ‘28, Milana Lezondra ’28, Sebastian Gacek ‘25, and Shubhik DebBurman, Neuroscience Department and Biochemistry & Molecular Biology Program, Lake Forest College, Illinois, 60045

Parkinson’s Disease (PD) is a common neurodegenerative disorder with its primary pathology being the selective death of midbrain substantia nigra neurons linked with the presence of Lewy bodies composed mainly composed of misfolded aggregated α-synuclein. Early-onset familial PD is well linked with six α-synuclein mutants that are well studied (A30P, E46K, H50Q, G51D, A53T, A53E), but three more recently discovered α-synuclein mutants (A18T, A29S, and A53V) linked with familial and sporadic PD are less well understood. Using our budding yeast (S. cerevisiae) model, we have recently found that these three newer mutants, while toxic to varying degrees, are surprisingly never more so than wildtype α-synuclein, with A29S being the least toxic and aggregated among them. Here, we have characterized these three mutants further by assessing 1) whether the loss of the original amino acid or the gain of the mutant amino acid (T, S, or V) is key to each mutant’s toxicity; 2) the effects on α-synuclein toxicity and aggregation when combining them; and, 3) the effects of altering known α-synuclein post-translational modifications (acetylation, SUMOylation, phosphorylation) on their toxicity. We report that for both A18 and A53 sites on α-synuclein, the loss of alanine is key to driving their individual toxicity. The A29 site is more complex, and it is the most toxic when substituted with arginine (R) and Threonine (T). Interestingly, for all three sites, some acidic substitutions (A18E, A29E, A53D) can reduce alpha-synuclein toxicity. When we assessed double (A18T/A29S, A29S/A53V, A18T/A53V) and triple (A18T/A29S/A53V) combinatorial mutants, we found out that A29S dominated over both A18T and A53V significant reducing their toxicities, indicating that the A29 position may be particularly important, especially when combined with A53. Together, our findings help with understanding how each of these three rare mutants may generate neurotoxicity that can explain underlying disease pathogenesis.

Aqueous Hydroxylation of Aryl Halides and Optimization of Tandem Oxidation of Benzyl Alcohols Under Air

Mariam Beshara ‘26, Haylee P. Christopher ‘27, Gwendolyn A. Jones ‘26, Dr. Erica E. Schultz

Abstract: This research project aims to optimize an oxidation-hydroxylation one-pot procedure to convert halobenzyl alcohols into hydroxybenzaldehyde derivatives under aerobic conditions using water as the primary solvent. The products produced by this reaction are important for pharmaceuticals, agrochemicals, and other industrial applications. By using Green Chemistry Principles, this study explores reaction conditions (catalyst, base, temperature, time, and organic co-solvent), to yield desired products with a decreased environmental impact. A comprehensive hydroxylation substrate scope was investigated, probing electronic and steric parameters. Additionally, mechanistic studies were conducted on both the hydroxylation and oxidation reactions to better parameterize the transformations. High-performance liquid chromatography (HPLC) and proton nuclear magnetic resonance (¹H NMR) spectroscopy provide quantitative data and structural analysis. The optimized hydroxylation conditions give phenols in up to >95% yield. Kinetic time course data on the benzylic alcohol oxidation to aldehydes give information about sequence of the tandem operation. This work will be applied to develop a more effective protocol.

Visuomotor Learning Across Limbs: Central Deficits Following Unilateral ACL Injury

Javier De La Cruz ‘27 and Dr. Shawn Flanagan, Center for Lower Extremity Ambulatory Research, Rosalind Franklin University of Medicine and Science

Anterior cruciate ligament (ACL) injury is known to disrupt motor control, but its effects on skilled visuomotor learning are not well understood. In this study we used a novel visuomotor reaction test to assess response time, accuracy, and motor learning across legs in individuals with and without ACL injury. Eighteen participants (10 ACL- injured, 12 controls) completed three 40-trial sets on a four-point lower extremity reaction platform, including a flipped stimulus-response condition to increase task complexity. Reaction metrics were paired with perceptual surveys, hydration status, and electromyographic (EMG) recordings to capture neuromuscular performance. Initial group comparisons revealed no significant differences in average response times, contact times, or error rates between injured and uninjured legs or between groups. However, single trial analysis (STA) revealed deeper insights. Controls showed greater and more consistent improvement in response times over 120 trials, particularly in the non-dominant leg, achieving greater improvement than ACL participants. In contrast, ACL-injured individuals exhibited limited learning in the injured leg and required more trials to reach steady state performance in the uninjured leg. Performance variability was elevated in both legs post injury, with notable deficits even in the typically dominant, uninjured limb. Together, these findings suggest ACL injury impairs bilateral visuomotor learning and adaptability, extending beyond immediate mechanical deficits. Reduced trial-to-trial improvement and increased response variability indicate persistent neuromotor disruption, underscoring the need for rehabilitation approaches that address bilateral cognitive-motor integration.

Investigating ER stress markers in Drosophila melanogaster with the knockdown of subunit four of the ER membrane complex (EMC) in glial cells.

Monique Dirzo ‘26, Otoha Tatami ‘24, Salma Abdelkhalek ‘26, Maria Jose Orozco Fuentes ‘24, Ines Riojas ‘26, Rebecca Delventhal Ph.D., Department of Biology and Neuroscience, Lake Forest College, Lake Forest, IL, 60045

The endoplasmic reticulum (ER) plays a crucial role in ensuring the quality control, folding, and insertion of membrane proteins, while also maintaining cellular homeostasis in eukaryotic cells. Within the ER membranes, the endoplasmic reticulum membrane complex (EMC), composed of 8-10 subunits, supports key ER functions. This complex is highly conserved between yeast and humans, but its range of functions in specific cell types remains poorly understood. Our lab examined the effects of glial cell EMC4 knockdown (EMC4KD) using RNA interference, and we found that Drosophila melanogaster exhibited delayed development, severe locomotor impairments, and a dramatically shortened lifespan of 5-6 days. Additionally, we observed molecular changes, including protein aggregation, in EMC4KD flies, suggesting the presence of ER stress. To further understand the pathways impacted by EMC4KD, we employed Western blotting and quantitative PCR (qPCR) to assess additional biological indicators of ER stress. We observed specific alterations in gene expression and protein levels involved in downstream pathways following EMC4KD. These findings help clarify whether ER stress caused by EMC4KD interacts with other stress pathways or organelles and offer insights into how glial cells activate mechanisms to preserve cell homeostasis.

Glial-specific function of the Endoplasmic Reticulum Membrane Protein Complex (EMC): distinct roles of individual subunits

Martin Ettlin Cuitiño ‘27, Maria Jose Orozco Fuentes ’24, Otoha Tatami ’24, Inés Riojas ’25, Rebecca Delventhal Ph.D., Department of Biology and Neuroscience, Lake Forest College, Lake Forest, IL 60045

The endoplasmic reticulum (ER) is an organelle critical for modifying, packaging, and inserting membrane proteins into the cell. The ER membrane protein complex (EMC), composed of 8–10 subunits, facilitates these processes. Malfunctions in several EMC subunits have been implicated in a range of human pathologies, including neurodegenerative diseases, visual impairments, metabolic disorders, and certain cancers. Previous findings from our lab demonstrated that fruit flies (Drosophila melanogaster) with a genetic reduction of EMC subunit 4 specifically in glial cells exhibited delayed development, severe locomotor impairments, and a dramatically shortened lifespan of 5–6 days compared to the typical 2–3 months. To investigate whether these effects were unique to EMC4 or if other EMC subunits are similarly required for glial cell function, we performed genetic reductions of additional EMC subunits. Surprisingly, we found that knockdowns of all tested subunits, except EMC3,generally resulted in normal development, lifespan, and locomotion, though knockdown of some subunits did show some sex-specific effects. These results suggest varying functional roles among EMC subunits. To further validate and explore these findings, future research will focus on measuring subunit levels in glial cells to better understand if the degree of reduction differs for each EMC subunit. We will also measure proteins whose production is impacted by each EMC subunit’s knockdown in glial cells to identify the subunit-specific client proteins for the EMC. Our findings emphasize the importance of understanding the distinct roles of each subunit, as some may be more required than others for specific EMC functions, such as transmembrane protein insertion, that are critical for glial function.

Perceptions of stress and aging in older adults by sexual identity and smoking status

Charlotte Flood, ’27, Vanessa Y. Fishel, BS, Nancy C. Jao, PhD, & Brian A. Feinstein, PhD; Department of Psychology, Rosalind Franklin University, North Chicago, IL 60045.

Older adults who smoke may use smoking to cope with unique aging-related stressors and discrimination. Additionally, sexual minority (SM) older adults face additional stressors and discrimination (e.g., ageism in the LGBTQ+ community). However, studies have not examined how stress and aging concerns may differ among older adults based on smoking status and sexual identity. We conducted a secondary analysis of the Columbus Healthy Aging Project, a cross-sectional survey of older adults (N=749, aged 50-88 years) in Columbus, Ohio. Four groups based on SM identity and smoking status (SM/Smoking, SM/Non-Smoking, Het/Smoking, Het/Non-Smoking) were compared on perceived stress, aging discrimination, and aging concerns using ANOVAs with Games-Howell post-hoc tests. Results indicated that SM/Smoking, SM/Non-Smoking, and Het/Smoking participants reported higher levels of stress, aging discrimination, and aging concerns compared to Het/Non-Smoking participants. SM/Smoking participants reported higher aging discrimination than SM/Non-Smoking participants, while Het/Smoking participants reported higher aging concerns than Het/Non-Smoking and SM/Non-Smoking. Results suggest that unique psychological stressors in older adulthood may be influenced by interactions between sexual identity and smoking status, raising questions about the relative contributions of each in understanding age-related challenges. Additional research is needed to understand how to best treat stigmatized groups of older adults (e.g., SM older adults and those who smoke) in healthcare settings.

Modifying Environmentally Persistent Compounds into Derivatives Bacteria Can Metabolize Under Biocompatible Conditions.

Jayla G. Freeman ‘28, Rachel S. Weiser ‘28, Karen P. Gomez, and Dr. Erica E. Schultz, Department of Chemistry, Lake Forest College, Lake Forest, IL 60045.

Organic compounds, which make up the majority of pharmaceutical agents, are a source of water pollution. Many organic compounds are not removed during the water treatment process. Water treatment relies on bacteria to remove organic compounds, but many pharmaceuticals evade degradation.  By redesigning traditional organic chemistry reactions to be non-toxic to microbial cultures (biocompatible), we aim to modify environmentally persistent pharmaceuticals (EPP) in the presence of living bacteria to encourage degradation. The reaction we targeted was the Pd-catalyzed reduction of C-Cl and NO₂ groups to C-H and NH₂, respectively. Using a specific bacterial community, mixed bacteria, to mimic a wastewater treatment facility (WWTF), we performed these reactions on organic compounds that share functionality with known EPPs. The product of these initial reactions can then be metabolized by mixed bacteria. We monitored the progress of our reaction with high performance liquid chromatography (HPLC). Reactions were run over the course of 48 hours, in which they were incubated and shaken at 30 °C to maintain the living bacterial cultures. Cultures were grown in M9 minimal media and Stanier’s Broth, to observe the metabolic capabilities with and without the presence of glucose as a carbon source. Progress was made toward coupling the Pd-catalyzed reaction with microbial metabolism for the degradation of these small molecules. After 48 hours, we saw full conversion of starting material into aniline along with living bacterial cultures, showing effectivity and biocompatibility of the reaction.

Detecting Asset Price Bubbles: An Early Warning System for Market Instability

Anastasia Galkova ’26 and Dr. Tilahun Emiru, Economics Department, Lake Forest College, Lake Forest, IL 60045

This project develops an early warning system for speculative asset price bubbles in U.S. equity markets using a hybrid methodology that combines rule-based detection and supervised machine learning. A custom labeling framework is applied to a decade of daily data from S&P 500 stocks to identify bubble periods and their preceding buildup phases. A rich set of technical indicators is engineered to capture momentum, volatility, volume, and trend-following signals. Several classifiers are trained and evaluated, including Logistic Regression, Gradient Boosting, and Random Forest, using time-aware cross-validation per ticker. The Random Forest model with a reduced feature set achieves the best balance between bubble recall (0.79), early warning recall (0.78), and precision (0.34), outperforming simpler models that fail to capture non-linear market behavior. The results demonstrate that interpretable, real-time models can be built to identify speculative activity with both robustness and foresight, though limitations around label accuracy and market complexity remain. Future research may improve these systems by integrating fundamental data, dynamic labeling strategies, and reinforcement learning for adaptive threshold tuning.

Alternative Lawns at Lake Forest College

Emma O’Malley Galvan ‘25, Giorgia Maran ‘28, Alexandra Anderson, Dr. Camila Pizano, Biology Department, Lake Forest College, Lake Forest IL 60045, and Dr. Rebecca Barak, Chicago Botanic Garden, Glencoe IL, 60022.

The American green grass lawn is often thought of as the default: framing households across the country, consuming 30-60% of all American home, business, and educational facility water use - making it the largest irrigated crop in the country. Turf is non-native and non-pollinator friendly, posing the question as to why we aren’t utilizing native, sustainable, and low-maintenance options instead. The Chicago Botanic Gardens, in collaboration with the Chicago Park District, have started an initiative by researching alternative native lawn compositions. The campus of Lake Forest College is also comprised of swaths of non-native green grass lawn, making it a contender for improvement. This study aims to integrate a composition of short growing native Midwest perennial plants in experimental plots on campus, as an example for potential landscaping alternatives at Lake Forest College. In collaboration with Dr. Pizano and Dr. Becky Barak with the Chicago Botanic Gardens, this project has utilized greenhouse space to grow plugs from seed, 1,040 of which were planted into experimental plots in the field this September and October, 2025. Half of the experimental plots will serve as a control, while the remainder are treated with compost. We expect to see a significant difference between the control and compost-treated plots. While prairie restoration in the Midwest has delivered insightful results, an alternative lawn project gives insight on intermediates that are feasible for the average homeowner, and for widespread use around our own campus, giving a future space for our own compost to go to good use.

Kaposi’s sarcoma-associated herpesvirus (KSHV) hijacks host water channel proteins to regulate KSHV reactivation and induce autophagy in infected cells.

Viridiana Guillen ’27, Christopher Kywe, Neelam Sharma-Walia, PhD Department of Microbiology and Immunology, Rosalind Franklin University of Medicine and Science, North Chicago, IL

Kaposi’s Sarcoma-associated Herpesvirus (KSHV) is a virus that has not yet been fully characterized within medical research. Identified in 1994, it continues to be studied for its main functions, particularly regarding its mechanisms of transmission between hosts. KSHV is characterized by two distinct life cycles that contribute to its survival and propagation: the latent and lytic cycles. During latency, the virus remains inactive until it transitions to the lytic cycle, at which point viral replication and dissemination occur. KSHV relies on several host proliferation regulators, including water channel proteins called aquaporins (AQPs), especially AQP3. It is a protein found in most living organisms that facilitates the transport of water and glycerol. AQP3 is involved in microbial pathogenesis and inflammation-associated responses, which has led to interest in their potential as therapeutic targets. Here, we demonstrate that 1) KSHV latent gene v-Cyclin transduction induced AQP9 as compared to AQP3. KSHV latent gene v-FLIP transduction did not induce either AQP3 or AQP9 as per Western botting. 2) KSHV infected primary effusion lymphoma cell lines BCBL-1 and BC-3 expressed higher levels of host AQP3 as compared to control BJAB cells. BCBL-1 and BC-3 also expressed viral latent (ORF73) and lytic (ORF45) proteins. 3) DFP00173 (DFP), is a potent and selective small-molecule inhibitor for AQP3. DFP treatment in KSHV infected BCBL-1 cells induced lytic reactivation as observed by high level of KSHV lytic protein ORF45. 4) AQP3 inhibition by DFP treatment in KSHV infected BCBL-1 cells induced autophagy protein LC3. 5) KSHV infection in human umbilical vein endothelial cells (HUVECs) stimulated the expression of AQP3. Lytic cycle induction therapy is promising, and research is ongoing to identify more effective lytic inducers. Further investigation is warranted into the potential of AQP3 inhibitors as a therapeutic intervention in controlling and eliminating KSHV latency in its associated cancers.

Multimodal communication in gladiator meadow katydids   

Authors: Chante Jacobs ‘27, Thalia León-Rodríguez ‘27, Jared Swensen ‘27, Flavia Barbosa, Biology Department, Lake Forest College, Lake Forest, IL 60045

Multimodal communication occurs when signals are conveyed across multiple sensory modalities. The different modalities may provide redundant or different information to receivers. Katydids (Orthoptera: Tetigoniidae) communicate through acoustic signals generated when they rapidly rub their wings together. Some species exhibit multimodal communication, also producing tremulations, where vibrations are produced that move along the plant. Tremulation behavior is much less studied, partly due to it not being audible and often being difficult to detect. It was previously unknown whether the gladiator meadow katydid, Orchelimum Gladiator, engaged in tremulation behavior, but they were known to call.   We hypothesize that calls and tremulations contain different information and will therefore be used in different contexts. We collected O. gladiators from Middlefork Savanna Forest Preserve (Lake Co., IL) and recorded while on a plant extracted directly from the field. There were three treatments for trials: males with other males, males with females, and solitary males. Each male was recorded as the focal for each treatment in randomized order. During trials, both males and females performed tremulations, which is the first record of this behavior in this species.  We expect tremulations to be observed primarily during courtship ritual behaviors, and we observed this behavior in both male-female and male-male trials. We also expect calling behaviors to differ based on the social context.

Performance of Haptic-Enhanced Canes with Varying Sensor Configurations in Real-World Navigation

Amal Khan ’28 and Frederick R Prete, Ph. D, Biology Department, Lake Forest College, Lake Forest IL 60045

Approximately 23 million people who are blind or low vision (B/VI) use mobility canes. Although effective, traditional canes cannot detect obstacles beyond their tip. We evaluated three haptic-enhanced canes, each with different numbers and arrangements of infrared time-of-flight (ToF) sensors that triggered vibratory feedback in the handle. Volunteers wearing sleep shades (N = 6) navigated a pathway with cardboard box obstacles. Each participant completed four trials: one without haptic feedback and three with haptic feedback, each using a different cane prototype. The prototypes included: (1) a single forward-facing ToF sensor (VL53L1X) linked to a vibrating motor controlled by a DRV2605 haptic driver, (2) two side-facing ToF sensors angled ~30° from the midline with outputs modulated through the same driver, and (3) a forward-facing plus two side-facing sensors integrated with an inertial measurement unit (IMU) regulating vibration output. Performance was scored as “identify” (detected prior to contact), “bump” (side contact after late detection), or “collision” (direct contact). Without haptic feedback, participants identified 0% (of 40 possible encounters per subject) and collided/bumped in 44%. In contrast, the 1-sensor cane identified 58% with 7% collisions/bumps, the 2-sensor cane identified 53% with 6% collisions/bumps, and the 3-sensor cane identified 70% with 16% collisions/bumps. Results show haptic feedback improved obstacle detection and reduced collisions. Participants preferred the single-sensor and three-sensor canes due to less ambiguous feedback near obstacles. In conclusion, integrating haptic feedback into mobility canes enhances obstacle detection and reduces collisions, with single-forward sensor configuration providing the most consistent improvements in navigation safety.

Modulating Inflammation in Alzheimer’s Disease via Inflammazome Inhibition

Yuliia Kulchytska ‘28, Sonia Arora, Mike Milovanovic, and Dr. Robert Marr, Department of Neuroscience, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60045

In recent years, the role of inflammation in Alzheimer’s disease (AD) progression has become increasingly evident, leading researchers to explore different methods through which they can control and inhibit inflammatory pathways. One such pathway is the NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome, which activates proinflammatory cytokines such as interleukin-1β (IL-1β) and IL-18. In AD models, elevated levels of IL-1β and caspase-1 have been found compared to controls (non-AD). Our lab aimed to develop a dominant-negative (DN) inhibitor of NLRP3 signaling overcome limitations associated with localized delivery. To enhance delivery and blood-brain barrier (BBB) permeability, the inhibitor was tagged with a low-density lipoprotein receptor binding site from apolipoprotein B (apoB), resulting in the final lentiviral construct: LV-GFP-apoB-ASC-DN. After generating the lentivirus, we used it to transduce a monocyte-derived cell line (THP-1) and assessed its effect on IL-1β production via ELISA. The results showed a significant reduction in IL-1β levels, indicating successful inhibition of the inflammasome pathway. However, while statistically significant inhibition was found in the monocytes.

Presynaptic and Cytoskeletal Changes in the Striatum and Cortex of Auxilin Knockout Mice

Mafe Parra Lancheros ‘27, Noémie Arrivé, Dr. Vidyadhara D J

Rosalind Franklin University of Medicine and Science, North Chicago, IL 60045

Parkinson’s Disease (PD) is a neurodegenerative disorder that causes motor impairments and non-motor symptoms such as cognitive decline. We used an auxilin knockout (KO) mouse model that mimics key features of PD by carrying a deletion of the DNAJC6 gene, which encodes the presynaptic protein auxilin. Mutations in DNAJC6 have been linked to early-onset PD due to impaired clathrin-mediated synaptic vesicle recycling. A previous proteomics study in auxilin KO mice suggested axonal dysfunction, including the upregulation of neurofilament light chain (NFL). We investigated axonal integrity across brain regions involved in motor and cognitive functions, namely the striatum and cortex, respectively. Immunohistochemical analysis revealed dopaminergic axonal deformities and neurofilament disorganization in the striatum of auxilin KO mice, indicating early cytoskeletal damage that may contribute to motor symptoms. In the cortex, overall NFL expression appeared unchanged between wild-type and auxilin KO mice. However, layer-by-layer analysis revealed significantly higher NFL levels in cortical layers 2/3 and 4 of 3-month-old auxilin KO mice. These differences were no longer evident at 9 months of age, which we believe is due to compensatory mechanisms or the loss of neurons with degenerative phenotypes at this later stage. To investigate underlying mechanisms, we conducted complementary proteomic analysis of purified synaptic vesicles from auxilin KO brains. This revealed downregulation of key proteins involved in dopamine signaling, vesicle cycling, and axonal transport. Future studies will aim to determine whether the layer-specific cortical changes and regional differences between the dorsal and ventral striatum reflect underlying neuron-specific or circuit-specific vulnerabilities contributing to PD pathology.

Tuberculosis Mycosin proteases as an antibiotic Target: Using Enzyme purification, kinetics and molecular modeling to identify specific inhibitors Kinetics Define Inhibitor Potency and Specificity

Jeremy Levin ‘26, Alvaro Arroyo ‘26, Martius Bautista, Jaila Philips, Juanita Muigai, and Dr. William Conrad, Lake Forest College, Lake Forest, IL 60045

MycP1 and MycP3 are subtilisin-like proteases located in the periplasmic membrane. Genetic deletion of either protease severely attenuates tuberculosis’ survival in the host. MycP1 mediates virulence factor export through the ESX-1 secretion system. MycP3 mediates the export of molecules involved in iron acquisition by the mycobacterium. Because MycP1 and MycP3 are essential for Mycobacterium tuberculosis survival, they represent potential drug targets. We hypothesized that broad-spectrum protease inhibitors could be modified to block MycP1 and MycP3 activity while sparing distantly related human proteases. To test feasibility, heterologously expressed MycP1-6xHis was purified using an adapted fast protein liquid chromatography (FPLC) protocol, yielding a ~45 kDa product confirmed by gel electrophoresis and Western blot. MycP1-6xHis activity was assessed using PNPA as a substrate, and activity exceeded the spectrophotometer’s detection range, confirming both high activity of the purified sample. Protease kinetics and inhibition was first modeled using α-chymotrypsin with the broad-spectrum inhibitor PMSF, which reduced enzymatic activity, exhibiting an increase in Km while Vmax remained unchanged, consistent with competitive inhibition. Swissdock modeling depicted PMSF binding the chymotrypsin active site. Modified PMSF is predicted to bind more tightly to the active site. Collectively, these results demonstrate successful purification of active MycP1 and validate the use of related proteases to model inhibitor interactions, establishing a foundation for the development of selective MycP1 inhibitors as potential leads for tuberculosis drug development.

Investigating the induction of lipid accumulation by antipsychotics in the MO3.13 cell line

Luiza Husemann Vieira Marion ’26, Vitor Ikeda Ito Silva, Caio Henrique de Souza Ferreira Berdeville, and Dr. Daniel Martins-de-Souza. UNICAMP Laboratory of Neuroproteomics. 

Antipsychotic medications are widely prescribed for the treatment of psychiatric disorders. While their mechanisms of action in the brain are well understood, their metabolic side effects are not fully understood. Lipid synthesis in oligodendrocytes is essential for the formation and maintenance of myelin, a structure composed of about 70–80% lipids that provide both structural stability and functional properties that enable rapid saltatory conduction of electrical impulses. Lipid accumulation, not common in the central nervous system under normal conditions, has been linked to the development of metabolic syndromes and has been observed in patients who undergo long-term antipsychotic treatments. This study investigated the induction of lipid accumulation by antipsychotics in the human oligodendrocyte-derived MO3.13 cell line, a model system frequently used to study lipid metabolism under drug treatment conditions and glial cell responses in inflammatory conditions. Cells were divided into three experimental conditions: blank (no treatment), Quetiapine treatment (at therapeutically relevant concentration), and Olanzapine treatment (at therapeutically relevant concentration). Lipid accumulation quantification was done through the Oil Red Imaging-based quantification protocol. Contrary to what we expected, results did not demonstrate a drug-specific increase in intracellular lipid accumulation in the treatment conditions, suggesting that antipsychotic exposure alone may be insufficient to alter lipid storage in MO3.13 cells, highlighting the importance of experimental context in studying antipsychotic-induced metabolic effects and suggesting that additional cellular or systemic factors may be required to trigger lipid dysregulation.

The Sex-Specific Effect of Unpredictable Fear on Neuronal Activity in the Rat Bed Nucleus of the Stria Terminalis (BNST)

Ryan Medich ’28, Corein Eaton Jr., Susan L. Olson, and Joanna Dabrowska, Center for the Neurobiology of Stress Resilience and Psychiatric Disorders, Rosalind Franklin University of Medicine and Science

Post-traumatic stress disorder (PTSD) and anxiety disorders are more common in women than men. However, the biological mechanisms underlying these sex differences are not well understood. The bed nucleus of the stria terminalis (BNST), a brain structure within the extended amygdala critical to fear and anxiety in both humans and rodents, has been shown to be hyperactive in PTSD patients. Corticotropin releasing factor (CRF) neurons within the dorsolateral BNST mediate sex-specific differences in anxiety potentiated startle (APS) following unpredictable fear conditioning in rats. Specifically, activation of CRF neurons within the dorsolateral BNST (BNSTdl) have been shown to reduce non-cued fear – anxious arousal – in female rats, depending on phase of reproductive cycle. Here, we aim to determine the cellular and molecular markers of CRF neuron activation within the BNSTdl following unpredictable fear recall in a sex and reproductive cycle phase-dependent fashion. To accomplish this, we performed behavioral testing utilizing the aforementioned APS paradigm with eight male and eight (4 control and 4 stressed rats in each group) reproductive phase tracked female CRF-Cre transgenic rats (Cre-recombinase under CRF promoter). These rats were injected during stereotaxic surgery with a viral vector in order to express mCherry reporter protein specifically in the CRF neurons of the BNSTdl. Brains were collected after the second recall test, followed by immunofluorescent staining for striatal enriched protein tyrosine phosphatase (STEP), which has been shown a unique marker of CRF neurons in the BNSTdl in male rats as well as early growth response protein 1 (Egr1), a transcription factor commonly used as a cellular activation marker. Our results indicate that Egr1 is expressed in the BNSTdl following APS in male and female rats. When analyzed for co-expression, male rats had showed higher coexpression levels of STEP and Egr1 compared to females, independent of treatment group. Our results show distinct cellular makeup of CRF/STEP neurons activation of the BNST in male and female rats, which might underlie sex-specific responses to unpredictable fear conditioning in the APS.

Social Isolation Increases Anxiety in Female Mice Leading to Increased Risk of Alzheimer’s Disease

Kaia Mismash ‘27, Lainey Toennies, and Dr. Holly C. Hunsberger, Center for Neurodegenerative Disease and Therapeutics, Rosalind Franklin University of Medicine and Science, 60045

Alzheimer’s Disease (AD) is a neurodegenerative disease affecting over 7 million Americans as of 2025, with females disproportionately affected. Behaviorally, AD is characterized by neuropsychiatric symptoms and cognitive decline. Biologically, AD patients show an accumulation of amyloid plaques and tau tangles with cell loss and brain shrinkage. AD has been on the rise since the COVID-19 pandemic which resulted in social isolation for many people around the world. In fact, social isolation is a significant risk factor for AD. Therefore, there is a need to understand how acute and chronic isolation accelerates AD pathology. To better understand how isolation changes behavior and brain-wide circuits involved with anxiety and cognition, we isolated or group housed control and AD mice for 5 days after a stressful event (3-shock fear conditioning). We then re-exposed mice to the same context to measure memory retention. One hour later, brain tissue was taken for analysis of cell activation in the hippocampal and amygdala regions, both of which are involved in memory and anxiety. We hypothesize that isolation will differentially impact males and females.

CRISPLD2 Overexpression in Th17 Cells Decreases IL-17A In Vitro and Delays Disease Onset in Experimental Autoimmune Encephalomyelitis

Minal Mohammed ‘26  , LP Adhikari², Kristen M Patterson², Joseph M Reynolds² Lake Forest College, 60045, USA² Center for Cancer Cell Biology, Immunology, and Infection, Rosalind Franklin University of Medicine and Science, North Chicago, IL, 60045

Cysteine-rich secretory protein LCCL Domain-Containing 2 (CRISPLD2) plays a crucial role in immune inflammation and regulation by inhibiting the production of pro-inflammatory cytokines in monocytes and mice. This study investigates CRISPLD2 overexpression (OE) in an in vitro T-helper 17 (Th17) cell model and in vivo experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS). MS is an autoimmune disease that is characterized by migration of autoreactive T-cells in the central nervous system (CNS) and degeneration of healthy myelin. In this study, the CRISPLD2 gene is cloned into a plasmid vector pGEM-T Easy, followed by its insertion into the pCMMP-MCS-IRES retroviral vector. The CD4⁺ Th17 cells are then transduced with the vector to examine its effects on interleukin-17A (IL-17A). The culture of CD4⁺ Th17 cells isolated from secondary lymphoid organs overexpressing CRISPLD2 shows that CRISPLD2 OE leads to reduced IL-17A expression. We recently advanced to in vivo studies where the Th17 cells with CRISPLD2 OE are adoptively transferred to induce EAE in recipient mice. We observed that CRISPLD2 OE slightly delays the onset of disease, and induced mice had significantly reduced IL-17A levels. This data suggests that CRISPLD2 may be relevant to T-cell pathogenesis in MS. Future directions include more EAE experiments to ensure the reproducibility of the data and exploring the correlation of the CRISPLD2 gene with inflammation in other autoimmune diseases. Although we cannot currently conclude the role of CRISPLD2 in MS, further research will allow us to determine the possibility of therapeutic applications for MS patients.

Telomerase Expression Levels Increase During Meiosis in Tetrahymena Thermophila 

Shuntaro Nakamura ‘27, Lily Avila, Gwendolyn Geissler Victoria Kutkovska, and Karen Kirk, Biology Department, Lake Forest College, Lake Forest, IL 60045 

Telomeres, composed of repetitive DNA–protein structures at chromosome ends, preserve genome integrity during replication. Telomerase, the ribonucleoprotein that maintains telomeres, consists of the catalytic subunit TERT and the RNA template TER. While the regulation of telomerase activity during the cell cycle remains poorly understood, prior studies using Northern blot in the binucleate ciliated protozoan  Tetrahymena thermophila have shown increased TER expression during meiosis. Here, we report the first analysis of TERT mRNA expression during meiosis in T. thermophila using qPCR. We examined three meiotic stages: (1) the micronuclear crescent stage (prophase), (2) completion of meiosis, and (3) development of the larger macronucleus. TERT transcript levels were quantified relative to GAPDH and Actin reference genes, using RNA converted to cDNA from each stage. Our results show that TERT expression is markedly elevated during meiosis compared with the vegetative state. These findings suggest that both TER and TERT are regulated during meiosis, potentially linked to DNA double-strand break formation and repair processes characteristic of this stage.

Impacts of Positive vs Neutral Stimuli on Recognition

Veronica Novak ‘28, Yuliia Treviño ‘28, and Dr. Wentworth, Psychology Department, Lake Forest College, Lake Forest, IL 60045

Every person has the ability to recognize individual faces because of distinct and entirely unique facial feature combinations. Humans can do so in a fraction of a second regardless of how familiar the face may be. However, when exposed to too many faces at once, our ability to recognize individuals declines significantly. In an effort to assist this process, the brain can be exposed to other stimuli, such as mood-inducing media. We hypothesized that individuals exposed to positive stimuli would show better recognition memory and that we would also see higher P300 amplitudes for recognized previously seen (old) faces. To investigate more in-depth, we wanted to explore how positive and neutral stimuli (two specific videos) would help people’s ability to recall familiar faces. We recorded two types of data: participants’ accuracy in recalling old faces and their brain wave activity while they were performing the recall task. Our accuracy data was collected through the usage of E-Prime system, while our event-related potential (ERP), specifically looking at the component known as P300, was collected through the usage of an electroencephalogram (EEG), BIOPAC system. We found that the effect of mood on memory wasn’t statistically significant, p = .447. We also did not find a significant difference in P300 amplitudes for correctly recognized old versus new faces, p = .504, or in the overall difference in P300 between old and new faces, p = .183.  However, we did find a statistically significant result regarding P300 levels in response to incorrectly recognized old versus new faces, p = .033.

Implementing a course-based Alzheimer's APP proteolysis research experience for undergraduate neuroscience curricula

Aaron B. Oster ’26, Tamara Víquez Bolaños ’28, D. Blaine Moore, Ph.D, Neuroscience Department, Lake Forest College, Lake Forest, IL 60045

Course-based undergraduate research experiences (CURE) provide benefits to students by integrating fundamental laboratory techniques with course content. We investigated if implementation of a CURE model showcasing the amyloid hypothesis of Alzheimer’s disease (AD) could increase student knowledge of proteolysis and be adapted for broader use at undergraduate institutions. In Spring 2025 at Lake Forest College, a CURE was implemented in NEUR301: Neuron to Brain, an upper-level, semester-long core neuroscience course. CHO 695 cells (gift of Dr. Virginia Lee) stably transfected with the 695 amino acid variant of human amyloid precursor protein (APP) were treated with PMA for two hours to stimulate alpha secretase proteolysis. Conditioned media was harvested and cell lysates collected. BCA protein assay was used to measure total protein in lysate samples and served to normalize for secreted amyloid beta (Aβ) levels measured via a human Aβ ELISA. Normalized class data were pooled and analyzed with student’s t-test (two-tailed, heteroscedastic). PMA treatment lowered Aβ secretion by over 50% for the entire class (twelve pairs of students), indicating a shift in baseline APP proteolysis. Learning outcomes were assessed by surveys given pre- and post-CURE. Survey results indicated significant increases in student learning, including increases in (1) confidence in utilizing cell-based models of Alzheimer’s, (2) experience with cell- and molecular-based laboratory techniques, (3) interest in neurodegenerative diseases, and (4) confidence in critical thinking and writing skills. Because accessibility to CHO695 cells is limited, there may be challenges to the widespread adoption of this CURE model. We sought to determine whether commercially available CHO Pro5 cells would be a suitable substitute. Using UniProt and FASTA, we retrieved the amino acid sequences of APP isoforms (the 770, 751, 695 amino acid variants) for human and Chinese hamster APP. Sequence alignment via BLAST and Clustal Omega was conducted to assess differences in the Aβ region of APP at the epitopes targeted by the human Aβ ELISA antibodies. Sequence alignments indicated no significant differences in the APP isoforms, and significant conservation of the Aβ region of the APP isoforms, suggesting the use of the CHO Pro5 cell line could serve as a more accessible alternative for broader implementation of this CURE model at undergraduate institutions.

Visuomotor Transformations for Courtship Behavior in Drosophila

Gizem Ozturk ’26, Duncan Mearns, Ph.D, Mala Murthy, Ph.D, Princeton Neuroscience Institute, Princeton University, Princeton, NJ 08544

The transformation of visual sensory input into behavior is important for courtship behavior of fruit flies (Drosophila melanogaster). During courtship, male flies use social cues, such as the distance from and movement of females, to pattern song production, showing precise conversion of dynamic visual cues into motor outputs. Lobula Columnar cells (LC) relay visual information through central brain regions to Descending Neurons (DN), which drive behavior via outputs in the nerve cord. LC10a neurons encode visual features of females that guide the male’s movement during courtship. However, it is unclear how other visual features encoded in other LC types are combined with information from LC10a in the central brain to shape courtship behavior. Here we investigate how visual information flows from LCs through central brain neurons to DNs using the FlyWire Connectome, a whole-brain map of an adult fly. We have mapped all monosynaptic and disynaptic connections between LCs and DNs. We have identified strong disynaptic input from LC10a to DNa08 through the intermediate neuron CB0359. DNa08 is sexually dimorphic and thus likely to be involved in driving sex-specific behaviors such as courtship. Clustering cells by connectivity revealed that DNa08 is part of a larger class of DNs that share similar inputs. We are now performing silencing experiments to investigate the role of DNa08 and CB0359 in courtship. This work highlights the structure and reveals potential underlying neural mechanisms of visuomotor transformations in the Drosophila brain during courtship.

Investigating the Effects of Antibiotic & Probiotic Administration on Appetitive and Consummatory Phases of Alcohol Self-Administration. 

Olivia Pandazi ‘26 and Dr. Hannah Carlson, Neuroscience & Psychology Department, Lake Forest College, Lake Forest IL 60045

28.9 million people in the U.S. alone have been diagnosed with Alcohol Use Disorder
(AUD) in the past year. Although there has been extensive research into AUD, concrete
understanding, therapeutics, and solutions for these individuals are scarce. Intestinal dysbiosis, the imbalance gut microbiota, has become increasingly recognized as a correlate in many disorders and diseases such as Parkinson’s and Alzheimer's. This study aims to investigate how intestinal dysbiosis plays a role in AUD via the gut-brain axis. We are testing the hypothesis that anaerobic gut bacteria promote voluntary, and potentially appetitive, ethanol consumption and that their depletion will have an effect on baseline drinking. Long-Evans rats (n = 6) acquire lever-pressing training for access to 10 % ethanol on an FR-1 schedule at 30-seconds free access, then advance to a fixed-ratio-20 (RR20) schedule with 20-minute free access to generate a 7-day baseline of intake (mL) and dose (g kg⁻¹). Beginning July 2025, animals will receive four intraperitoneal injections of tigecycline, a broad-spectrum, anaerobe-directed antibiotic, spaced over two weeks while daily RR20 sessions continue. We predict antibiotic-induced dysbiosis will significantly reduce ethanol intake versus baseline. After one week post-antibiotic, rats will undergo an oral regimen of a multi-species probiotic formulated to restore anaerobic diversity; we expect a rebound toward baseline drinking. Fecal samples collected at baseline, post-antibiotic and post-probiotic time-points will be analysed by quantitative PCR for key bacterial taxa, and trunk blood will be assayed for acetate via a commercial colorimetric ELISA to couple microbial fermentation capacity to systemic metabolite availability. Correlation analyses will link taxonomic shifts and acetate levels to behavioral outcomes. Demonstrating reversible microbiome modulation of operant drinking would provide a platform for mechanistic studies. Future work will pair targeted microbiome manipulations with excitation of the vagal nucleus tractus solitarius via injections to delineate gut-to-brain pathways controlling alcohol reinforcement. Data collection is in progress; findings will hopefully be presented at the November 2025 Symposium For Neuroscience.

Developmental differences in fear: Shifts in BLA glutamatergic receptors and GABAergic neurons

Ash Peacock ’28, Rachel Parker, and Dr Nicole Ferrara, Center for Neurobiology of Stress Resilience and Psychiatric Disorders, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60045

Adolescents are more vulnerable to fear-related psychiatric disorders than adults, partially due to ongoing brain development. Fear-related psychiatric disorders are marked by heightened fear expression resistant to suppression, a feature common among adolescents. The basolateral subregion of the amygdala (BLA) plays a critical role in fear memory processes and matures throughout adolescence. Therefore, BLA maturation may be key to understanding developmental differences that may inform fear-related disorder vulnerability in adolescents. Within the BLA, two factors may account for developmental differences in fear: glutamatergic receptor expression and increased GABAergic neuronal function. GABAergic inhibition helps suppress BLA excitation and subsequent fear responses, while glutamatergic receptor expression is inversely related to fear memory expression in younger cohorts. We hypothesized that adolescents would show dysregulated glutamatergic receptor expression and lower indicators of GABAergic activity. To test this hypothesis, adolescent and adult rats were either fear conditioned or left in their home cage as a control. BLA tissue was then collected after a long-term fear memory test where the expression of NMDAR subunits and GABAergic synaptic scaffold, gephyrin, were quantified using western blotting. Consistent with prior work, we found that adolescents displayed a higher degree of freezing than adults. In the BLA, we found a developmental increase in the GluN2B subunit of NMDAR expression in both groups. We also found that BLA gephyrin was reduced in fear conditioned adults relative to homecage controls. These results identify two cellular mechanisms that are developmentally regulated, one of which may account for developmental differences in fear expression.

Working Color: Studying How Color Affects Learning and Engagement

Gaby Planta-Yap ‘28, and Dr. Wentworth, Psychology Department, Lake Forest College, Lake Forest, IL 60045

Color in educational materials has impacted learning in a multitude of ways. The use of color within educational material has shown better results on tests relating to the material, while learning materials in grey scale don’t produce the same results. These outcomes point to the possible correlation between student performance and colorful educational material. In past studies, time spent looking and eye-movement were used as measures of engaged learning. These methods were both utilized in the comparison between color and grey scale materials. I hypothesized that individuals would have more eye-movement (saccades), spend more time looking, and have better learning in the color condition than the grayscale condition. To study this, a textbook page was modeled after a college-level textbook page with the inclusion of color in the main title, subtitles, captions, and all imagery included. The data that was for this study was total number of saccades, total time spent looking, and test scores. Saccades and total time spent looking were both recorded using an eye-tracker and Tobii Pro Software. Test scores were recorded using a quiz based on the information on the textbook page. An independent samples t-test was run using means of the saccades comparing the color and grayscale conditions and produced a p-value of p= .771. The same was done for means of scores and produced a p-value of p=.154. Thus, saccades and scores did not have a statically significant difference in their means. However, a correlation matrix was carried out between the color and grayscale condition and produced a p-value of p=.055. Although not statistically significant, this p-value indicates the results of the color condition presented a strong correlation between times and scores of the participants.

Epstein-Barr Virus Mediated K63-Linked Ubiquitination Alters Host Cellular Signaling Networks

Marina Priovolos ‘27 and Dr. David Everly, Department of Microbiology and Immunology, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60045

Epstein-Barr Virus (EBV) is associated with several cancers, including Hodgkin’s lymphoma, Burkitt lymphoma, and nasopharyngeal carcinoma. A major way EBV contributes to oncogenesis is by manipulating the host proteins through ubiquitination, which regulates protein stability and signaling. Alterations in ubiquitination can disrupt cellular pathways and promote oncogenesis. The purpose of this project was to identify how EBV-related proteins induce different ubiquitin linkages. To address this, GST-tagged expression plasmids were transformed and expressed in E.coli Rosetta strains. Following protein induction and purification with glutathione bead pulldown assays, SDS-PAGE confirmed protein solubility, and Western blotting with linkage-specific antibodies was used to assess ubiquitin binding. This analysis would indicate a preference for K63-linked ubiquitin, with minimal binding for K48 and M1-linked chains. Since K63-linked ubiquitination is typically associated with signaling rather than protein degradation, these findings will help to identify EBV-associated changes in ubiquitination that alter host signaling networks. By uncovering linkage-specific interactions, this work provides insight into the molecular strategies EBV uses to promote cancer progression. Future studies aim to test these interactions in mammalian systems and explore their role in therapy development.

Exon-Exon Junction Primers Eliminate No-RT Crossing in Aspergillus nidulans

Authors: Wells Roney ‘28, Dawid Oleksy ‘26, Shuntaro Nakamura ‘27, Eva Mannsbart ‘28, Karen Kirk

Telomeres, composed of repetitive non-coding DNA at chromosomal ends, protect against sequence loss during replication. Telomerase, the enzyme that maintains telomere length, is a ribonucleoprotein consisting of the catalytic reverse transcriptase TERT and the RNA template TER. We are investigating TERT mRNA expression in the filamentous fungus Aspergillus nidulans to assess potential variation across its life cycle. In initial RT-qPCR experiments with conventional primers, amplification in no-RT controls indicated genomic DNA contamination. To overcome this limitation, we designed an exon–exon junction primer pair for the A. nidulans TERT gene using IDT PrimerQuest™. Our results demonstrate that these primers are specific, efficient, and successfully eliminate no-RT amplification. This optimized primer design improves measurement accuracy and will facilitate reliable analysis of TERT expression across developmental stages in A. nidulans.

Investigating the Mechanisms of Cortical Activity Modulation by Water Restriction and Circadian Rhythm

Aziza Saiyed ‘27, Sophia Cinquemani, Dr. Eun Jung Hwang, Department of Cell Biology and Anatomy, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60045.

In behavioral neuroscience, water restriction is a commonly used method for increasing motivation in animal models. A previous study found cortical neurons showed elevated levels of c-Fos and beta adrenergic receptor expression in water-restricted mice. C-Fos serves as a proxy for neuronal activation, while beta-adrenergic receptors are G-Protein coupled receptors (GPCRs) activated by norepinephrine, that is, linked to arousal and motivation. In the present work, we sought to further explore the connection between water-restriction motivation and increase in cortical activity, while controlling for potential confounds from circadian rhythms on c-Fos expression. To assess circadian effects, we performed a parallel experiment, investigating the amount of cortical activity during active and inactive phases in the mouse model. We utilized immunohistochemistry staining for detecting the amount of c-Fos and beta adrenergic receptor expression in cortical neurons, specifically focusing on the motor cortex and posterior parietal cortex. Overall, these experiments aim to uncover how internal motivation or circadian rhythm can drive norepinephrine-mediated cortical activation, which may play a crucial role in cortical plasticity and learning.

CO and CO₂ on Rh(111) surface

Sofia Strupovets¹, Daniel Killelea², Veronika Walkosz¹

¹Department of Physics, Lake Forest College, Lake Forest, IL
²Department of Chemistry, Loyola University Chicago, Chicago, IL 60660

The adsorption of CO and CO₂ on transition metals has been widely studied due to their importance as benchmark molecules in surface science, where they are used to probe metallic surfaces through the electronic structure and surface reactivity changes they introduce.  Using Density Functional Theory calculations within the Vienna Ab Initio Simulation package (VASP), we calculated the binding energies of CO and CO₂ at different sites on the Rh(111) surface.  Three different exchange-correlation functionals were employed to treat electron-electron interactions: Perdew-Burke-Ernzerhof (PBE), vdW-DF2, and optB86b-vdW functionals. The latter two include non-local correlation effects to capture dispersion interactions.  In addition, we explored CO₂ decomposition into CO and O using these functionals.  Finally, vibrational frequency calculations were performed for CO adsorbed on both the clean Rh(111) surface and the surface with subsurface oxygen to validate the structural stability of the optimized configurations. The calculated frequencies are compared to experimental observations and previous computational results to establish the accuracy and reliability of our theoretical approach.

Testing the Reality of Bias Intervention in a Politically Balanced Sample

Mia Hernandez ’27, Alyssa Dyson ’27, Nicole Pido’27, Sarah Tahir ’26, Sara Rush ‘26, and Dr. Emily Dix, Psychology Department, Lake Forest College, Lake Forest IL 60045

White individuals often dismiss or deny concerns about racism raised by Black individuals, which fuels ongoing interracial tension. In a two-part study, we examined whether the Reality of Bias Intervention (Dix & Devine, 2024) could reduce this dismissive tendency. The Reality of Bias Intervention teaches two core concepts previously found to decrease the tendency to dismiss or downplay bias concerns: (a) White perspectives on bias are limited, and (b) the effects of bias accumulate over time. Whereas previous work tested this intervention only among college students, the present study used a politically balanced national sample of White adults. In Part 1, participants were randomly assigned to read either the intervention or a control article. Immediately after reading the article, participants who received the Reality of Bias Intervention reported significantly higher levels of concern about discrimination than those in the control. One week later, in Part 2 (N=378), all participants encountered a problematic Reddit post arguing that Black people overreact about racism; we hypothesized that intervention participants should take issue with the post by downvoting (rather than upvoting) it, rating it negatively, and leaving a comment that defends Black people’s bias concerns. Consistent with hypotheses, the likelihood of downvoting (vs. upvoting) was significantly higher in the intervention condition compared to the control. Intervention participants also rated the article more negatively. Coding of comments is ongoing. This study suggests that the Reality of Bias Intervention is effective even in a politically diverse sample and has the potential for broader application.

Using Recurrent Neural Networks to Explore Fear Learning and Extinction in PTSD

^*Mio Takata’28, Takafumi Soda, Hayato Idei, Yuichi Yamashita

¹Department of Information Medicine, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-higashi-cho, Kodaira, Tokyo 187-8551, Japan

Post-traumatic stress disorder (PTSD) is a psychiatric condition characterized by intrusive recollections of traumatic events and avoidance of trauma-related memories. A key mechanism underlying PTSD is considered to be an impairment in fear conditioning: individuals fail to update previously learned associations between cues once linked to threat and their current safety. A representative computational account of fear conditioning is the Latent Cause Model (LCM), a Bayesian inference model where individuals infer latent causes behind observed events and switch between them depending on contextual changes. A central parameter of this model, α, illustrates the tendency to introduce new latent causes. Previous studies using a task—where participants learned the reliability of robots associated with monetary loss and later underwent extinction training— estimated α for each participant. Some findings linked higher α with lower avoidance symptoms in PTSD, while others reported the opposite, leaving the relationship inconsistent. These mixed results indicate a limitation of LCM: its inflexibility to capture the flexible dynamics and individual variability of learning. The purpose of this study is addressing this issue by applying recurrent neural networks (RNNs), which have greater potential to extract detailed mechanisms. We trained RNNs with three different architectures on artificially generated data and examined contextual representations in hidden layers. We then compared these activations with the α used in data generation, thereby exploring how RNNs learn and represent context differently from LCM. This approach potentially reveals diverse learning dynamics not easily captured by Bayesian models, offering new insights into fear-conditioning deficits in PTSD.

Reducing the Post-Hoc Fallacy

Jenna Rose Thomas ‘27, Paul Henne, Ph.D, Lake Forest College, Lake Forest, IL, 60045

People often commit the post hoc ergo propter hoc fallacy—the mistaken assumption that because one event happened after another, the first caused the second. In Experiment 1, we gave participants (N = 1500) 15 ordinary vignettes where an agent tried a treatment for a medical or health condition and then their condition either improved or did not change. We asked participants to what extent they agreed that the treatment caused the improvement and should be continued. Participants tended to commit the post-hoc fallacy: they agreed more with causal statements and recommendations in the improved condition relative to the unchanged condition. We found that people’s causal judgments fully mediated their recommendations. For our second experiment, we aim to reduce the post-hoc fallacy by encouraging people to imagine alternative actions.

The Effect of the 4-1BB:4-1BBL Axis and TAM receptor knockout on Splenic B Cell Activation

Laney Thumser ’26, Carolina Calôba, Barbara Gabrielle dos Santos, Taylor Anne Lyons, and Rahul Vijay, Center for Cancel Cell Biology, Immunology, and Infection, Rosalind Franklin University of Medicine and Science, North Chicago, IL, 60064

Malaria remains a global health issue because long lasting immunity is hardly ever induced after natural infection; consequently, chronic reinfection is a common occurrence. B cells play a critical role in the adaptive immune response to Plasmodium by producing antibodies and acting as antigen presenting cells to activate other immune cells. Studying B cell responses to Plasmodium is pivotal to understanding why long-lasting immunity is not induced. Here, I present an optimized protocol to stimulate the B cells ex vivo in murine splenocyte cultures. In pursuit of this, we titrated time, reagents, and various stimulatory molecules to obtain data sets that are both repeatable and interpretable. Briefly, we focused on studying the role of 4-1BB:4-1BBL axis, and TAM receptors on B cell activation. The 4-1BB:4-1BBL axis is an important co-stimulatory signaling pathway that plays modulatory roles in the immune response. We found that when splenic B cells from mice lacking 4-1BBL are stimulated, all downstream signaling molecules show reduced activation; in contrast, there is no difference in mice lacking 4-1BB. TAM receptors (Tyro3, Axl, and MerTK) are not extensively studied in the context of malaria but generally act as negative regulators of immune responses. We found that splenic B cells from MerTK knockout mice show decreased pCD79a, a key signaling molecule of the B cell receptor; in contrast, other signaling molecules do not show any significant difference from the wild type. This optimized protocol has since been utilized in the lab for assays investigating B cell activation under various conditions.

Investigating Concurrent Alcohol and Nicotine Drug Self-Administration in Rodent Models.

Juan David Vargas '28, Ghazal Mosleh '28, and Dr. Hannah Carlson, Neuroscience &Psychology Department, Lake Forest College, Lake Forest IL 60045

Polysubstance use is a growing public health concern, with nicotine and alcohol being among the most commonly co-used substances worldwide (Crummy et al. 2020). While extensive research has examined the neurobiological mechanisms underlying alcohol and nicotine use independently, the behavioral and motivational dynamics of their concurrent consumption remain poorly understood. This study aims to investigate how concurrent nicotine and alcohol administration influences voluntary intake, preference, and reward-related behavior in a rodent model. Adult Long-Evans rats (n = 7) are trained to lever-press for access to 10% ethanol or nicotine solution under a fixed-ratio (FR-1) schedule, allowing baseline assessment of individual preference for each substance. Once stable responding is achieved, animals transition to a concurrent access paradigm in which both ethanol and nicotine are available during self-administration sessions. Intake (mL), dose, and preference ratios are recorded to determine shifts in consumption patterns under co-administration conditions. Subsequent phases will assess how nicotine exposure alters alcohol preference and vice versa, revealing potential cross-reinforcement or modulation effects between the two substances. Data collection is currently ongoing; forthcoming analyses will examine intake trends and behavioral correlations across experimental phases. These findings are expected to advance understanding of polysubstance reinforcement mechanisms and inform translational models of comorbid substance use disorders. Results will be presented at the November 2025 Symposium for Neuroscience.

Modeling Glutamate Excitotoxicity in N2a Neuroblastoma Cell Line

Tamara Víquez Bolaños ’28, Aaron B Oster ’26, and D. Blaine Moore, Neuroscience Department, Lake Forest College, Lake Forest, IL 60045

Glutamate is the major central nervous system excitatory neurotransmitter, and a  key regulator of learning, memory, and overall brain function., Excessive glutamate release following acute brain injury, however, can trigger excitotoxic cell death. We had two main objectives related to modeling this phenomenon in vitro. First, we sought to establish for the first time in our laboratory the neuron-like Neuro2a (N2a) cell line. Once established, our next objective was to establish the conditions for excitotoxicity. The cultures were exposed to a range of glutamate concentrations from 0 mM to 500 mM by adding it to the culture media, followed by incubation for 24 hours. Cell viability was measured using the MTT assay and quantified with a one-way ANOVA followed by Tukey’s post hoc test. 10 mM and 100 mM of glutamate produced minimal excitotoxicity; concentrations of 200–250 mM resulted in approximately 50% toxicity, while 500 mM produced high levels of cell death. As such, we met our goal of establishing the N2a model system in the laboratory and determining an LD-50 for glutamate toxicity.  This baseline will guide our next steps, which focus on testing organic compounds that target serotonergic receptor-regulators of glutamate release and could help protect cells from excitotoxic damage.

Mapping the Connectivity of Cingulate Cortex Neurons Projecting to the Posterior Parietal Cortex

Keisha William ’27, Youjin lee, and Eun Jung Hwang, Center for Brain Function and Repair, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60045

Cortical connectivity plays a crucial role in shaping complex cognitive behaviors. Recent work has shown that neurons in the cingulate cortex (CC) projecting to the posterior parietal cortex (PPC) encode the outcome history of past choices, suggesting that the CC conveys history information to the PPC to drive history-dependent decision bias. However, how these CC neurons projecting to the PPC (CCppc) can encode outcome history remains unclear. As a first step toward addressing this question, we anatomically mapped the input sources of the CCppc neurons using a dual-recombinase viral tracing system in double-transgenic mice (lslGFP::fsfTdTomato). We injected a retrograde AAV expressing FLPo into the PPC, along with a retrograde AAV expressing Cre into the CC, thereby labeling upstream neurons of the PPC and CC, respectively. Our results identified that CCppc neurons are located approximately 0.5 mm anterior and 0.3 mm lateral to bregma, while the CC neurons in that coordinate receive diverse inputs from multiple brain regions including infralimbic cortex layer 6b, 5a, tenia tecta dorsal layer 3, lateral septa nucleus rostral layer 5 and prelimbic layer 2. These findings provide precise coordinates for future manipulation or recording in upstream areas of the CCppc neurons. This work establishes a foundation for dissecting the larger circuit mechanisms involved in history dependence in decision-making.

Panic on DOI: Investigating the effects of DOI on 5HT2A receptor activity during a panic response in rat model.

Elena Yoshovska ’28, Ronan McGuire ’28, Oliver Seder ‘28 & J.A. Rosenkranz, Center of Neurobiology of Stress Resilience and Psychiatric Disorders  & Discipline of Cellular and Molecular Pharmacology The Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064, USA

DOI (2,5-Dimethoxy-4-iodoamphetamine) is not currently classified as a schedule 1 drug; it is because of this that DOI has been gaining more and more recognition within scientific research. DOI is a psychedelic drug and a 5HT2A (serotonin-2A) receptor agonist. The 5HT2A is widely known for its role in various psychiatric disorders, in which antagonists are given to treat the symptoms. We focused on DOI’s effect during a panic state in a rat model. Behaviorally, we saw that the control group reacted quickly in a panicked state, whereas the experimental rats reacted at a slower rate due to the drug. We only used a low dose (0.4 mg/kg) of the drug as we weren’t focused on testing different dosages within this experiment. At a molecular level, we were interested in comparing the activity of the 5HT2A receptor between the PFC and amygdala in rats that were given the drug vs. the control rats. Based on the behavioral results, we aimed to find more 5HT2A activity, meaning more psychedelic experience, in the brains of the experimental rats than the control rats. In future experiments, we would compare the affects of the drug at different dosages. Instead of two groups, there would be three: one as a control, one with 0.4 mg/kg of the drug given, and one with 1.0 mg/kg. 1.0 mg/kg of the drug has been said to produce head shakes in rodent markers, a visible sign of hallucinations, which could be a focus within future research.

MindScribe: Authoring Cognitive Wellness Through a Declarative, On-Device iOS Architecture

Christopher Zimbizi ‘27 and Dr. Sara Jamshidi. Lake Forest College, Mathematics and Computer Science Department Lake Forest, IL 60045

Rising concerns over cognitive decline and the limitations of fragmented, cloud-dependent digital health tools highlight a need for private, user-centric applications. The difficulty lies in building a comprehensive tool that is both feature-rich and prioritizes user data privacy, empowering individuals to proactively manage lifestyle factors grounded in established wellness principles. This project addresses the architectural and implementation challenges of creating a comprehensive, offline-first native iOS application for tracking five key pillars of brain health: Sleep, Exercise, Nutrition, Stress, and Engagement. We developed MindScribe, an application architected using the Model-View-ViewModel (MVVM) pattern with a declarative user interface built in SwiftUI. The core of the approach is a robust on-device persistence layer, ensuring all user data is stored securely and privately, making the app fully functional without network connectivity. The software was engineered with a modular, feature-based file structure to ensure long-term maintainability and scalability. The result is a feature-complete prototype that successfully implements daily data logging across all five pillars. The application features interactive data visualization for weekly and monthly trends and includes a system for generating comprehensive, multi-page PDF health reports directly on the user’s device. This work demonstrates that a modern, declarative, on-device technology stack can be effectively leveraged to create a secure and feature-rich health management application. The architecture serves as a model for developing user-centric, privacy-first applications in the digital wellness space, proving that complex functionality does not require compromising user data ownership.