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

The 2024 Glassman Symposium will be held October 31 – November 1.

The Glassman Symposium Poster Session seen from a balcony above

Honoring Outstanding Student and Faculty, and Alumni Research in Behavioral and Life Sciences

The Brain Awareness Week Faculty/Student Symposium was renamed the Robert B. Glassman Memorial Brain, Mind, and Behavior Symposium in 2013 in honor of the late Professor of Psychology Robert Glassman, who played a leading role in developing Lake Forest’s popular neuroscience major.

The symposium consists of a series of talks given by Lake Forest College faculty and alumni on October 31 and an poster session where Lake Forest students and alumni will present their original research on November 1. 

October 31 – Faculty/Alumni Talks

7–9 p.m., Tarble Room, Brown Hall 

7:00 p.m. Welcome Remarks, Synapse

Hannah CarlsonHannah Carlson, PhD

Assistant Professor of Neuroscience & Psychology, Lake Forest College

“Tranq-Dope,” a Deadly Combination: Assessing the Behavioral and Pharmacological Impact of Combined Fentanyl and Xylazine

7:05 p.m.


Saul Bello RojasSaul Bello Rojas ’16, PhD

Postdoctoral Fellow, Oregon Health Sciences University

Development and Structure of Motor Control in Spinal Cord

7:25 p.m.


Catherine ReedyCatherine Reedy, PhD

Assistant Professor of English, Lake Forest College

Infected Brains and Pestilent Congregations in Shakespeare

7:45 p.m.


Sarah ApplebeySarah Applebey ’18

PhD Candidate in Neuroscience, University of Pennsylvania

Room for Dessert?: Sex Differences in the Brainstem Control of the “Dessert Stomach”

8:05 p.m.


D. Blaine MooreD. Blaine Moore, PhD

Professor of Neuroscience, Lake Forest College

“Molecular Scissors” and Alzheimer’s Disease

8:25 p.m.


8:45 p.m. Closing Remarks, Synapse

November 1 – Undergraduate and Alumni Research Poster Session

View 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, Midwestern University, Northwestern University, University of Minnesota, Illinois Institute of Technology, and Rush University.

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

Research poster abstracts

Alumni Abstracts

Glucagon-like peptide-1 receptor-based treatments for weight-loss: Impact of the estrous cycle in female rats

Sarah V. Applebey ‘181,2, Allison G. Xiao 1, Matthew R. Hayes 1, Neuroscience Graduate Group, University of Pennsylvania, Philadelphia, Pennsylvania, Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania

Successful new weight-loss drugs like Ozempic and Zepbound have transformed the treatment of obesity. This emerging class of drugs, known as glucagon-like peptide-1 (GLP-1) receptor agonists, act on GLP-1 receptors (GLP-1Rs) in the brain to increase satiation and suppress food intake. Notably, recent clinical trials indicate women are more sensitive to GLP-1R agonists, showing a greater percentage of weight loss compared to men. However, the mechanisms underlying these sex differences are unclear. In female rats, we recently showed that the estrous cycle (menstrual cycle equivalent) impacts messenger RNA expression of brainstem Glp-1r and endogenous Glp-1. Compared to males, brainstem Glp-1r and Glp-1 expression increased in estrous phases associated with estrogen signaling, proestrus and estrus. As GLP-1 signaling in the brainstem is necessary for the weight-loss effects of GLP-1R-based treatments, we hypothesized that animals in proestrus or estrus expression would demonstrate more sensitivity to GLP-1R agonists. Here, we evaluated the ability of the estrous cycle to moderate the food intake and weight loss effects of two GLP-1R agonists in female rats with obesity. Indeed, the effects of short-acting agonist liraglutide ( Saxeda) were potentiated during proestrus and estrus. Moreover, chronic semaglutide ( Wegovy) treatment, injected solely during proestrus or estrus produced significantly greater weight-loss compared to rats treated in other phases. Collectively, our findings reveal estrous-cycle dependent sensitivity to GLP-1R-based pharmacotherapies. As many patients receiving GLP-1R-based pharmacotherapies experience a regular menstrual cycle, clinical research is needed to determine whether physicians should consider menstrual cycle phase when designing treatment plans. NIH-DK137443.

Regulation of Neuronal Inflammation in an Experimental Autoimmune Encephalomyelitis Model via LAG3 Under-Expression

Allison Coffell ‘24, Joseph Reynolds, Kristen Patterson, Center for Cancer Cell Biology and Immunology, Rosalind Franklin University of Medicine and Science, IL, 60064, USA

Multiple Sclerosis (MS) is an autoimmune T-Cell mediated disease of the Central Nervous System (CNS) resulting in degeneration of healthy myelin. The immune checkpoint receptor, Lymphocyte-Activation Gene 3 (LAG3) is typically under-expressed in MS patients. This study elucidates the therapeutic potential of a LAG3-targeting antibody in reducing neurodegenerative virulence in an Experimental Autoimmune Encephalomyelitis (EAE) mouse model. LAG3 antibody-treated mice exhibit decreased levels of pro-inflammatory Interleukin-17A (IL17a) CD4 presenting T-cells within the brain as well as increased levels of LAG3 in the spleen. Scoring data revealed a slowed progression of symptoms in EAE mice treated with a LAG3 antibody. A transfer experiment revealed the preventative effect of shRNA silencing of LAG3 on EAE pathogenesis. These findings thus demonstrate the role of LAG3 deregulation in reducing neuronal inflammation and altering typical trajectory of MS symptomology in an EAE model.

Characterizing cold hypersensitivity in a mouse model of relapsing-remitting experimental autoimmune encephalomyelitis

Kamden T. Kuklinski ‘23, Manish K. Madasu, & Ream Al-Hasani, Center for Clinical Pharmacology, Washington University Pain Center, Department of Anesthesiology, Washington University School of Medicine in St. Louis, St. Louis, MO 63110

Approximately one third of patients who have been diagnosed with multiple sclerosis (MS) will develop a hypersensitivity to cold temperatures. Despite the relatively high frequency of this symptom’s occurrence, little is known about the neurochemical mechanisms that underlie this altered sensation. Recent studies, however, have implicated peripheral activation of the kappa opioid receptors (KOR) in cold hypersensitivity. To determine whether the KOR plays a role in cold allodynia associated with MS, we used a mouse model of relapsing-remitting experimental autoimmune encephalomyelitis (RREAE) to induce an MS-like pathology. We had selected this disease model over other models of MS since it causes a robust disease state that does not immediately inhibit motor activity. Once the disease state has been induced, the body weight and experimental autoimmune encephalomyelitis (EAE) score of each animal is assessed daily to monitor health. Cold hypersensitivity was assessed weekly using a cold plantar assay at either 3 or 10°C. Additionally, mechanical hypersensitivity was assessed using a von Frey assay. Through these tests, we show that diseased mice are made more sensitive to both cold and mechanical stimuli when compared to control mice. Sections of lumbar spinal cord were stained with Luxol Fast Blue (LFB) and Cresyl Violet (CV) to determine whether differential myelination was associated with induction of a worsened disease state. Further investigation of kappa opioid receptor signaling and its role in cold hypersensitivity could result in the development of novel therapeutics which specifically target this system to alleviate pain and discomfort. Funding: NINDS – R01NS123070,  NIH – R25NS130965

Student Abstracts

Investigating the tissue-specific impact of EMC4 knockdown on fertility and lifespan in D. melanogaster

Salma Abdelkhalek ‘26, Otoha Tatami ‘24, Rebecca Delventhal PhD, Department of Biology and Neuroscience, Lake Forest College, Lake Forest IL 60045

The endoplasmic reticulum (ER) and its membrane protein complex (EMC) are essential for maintaining cellular homeostasis, facilitating lipid biosynthesis, and ensuring the stability and integration of membrane proteins within the lipid bilayer. Given EMC4's role in development and longevity, exploring its impact on reproductive capacity is essential. EMC plays a key role in trafficking proteins and membrane proteins, which are vital for signaling to the ovaries and regulating fertility, thus a disruption in EMC function may impair reproductive tissues. To investigate the tissue-specific roles of EMC4, we knocked down expression of EMC4 on Drosophila melanogaster in different tissues and assessed the impact on fertility, fecundity, and lifespan. We focused on immune and metabolic tissues in young and aged flies, including hemocytes, the fat body, and insulin-producing neurons. Assessing the fertility and fecundity of flies revealed that a knockdown of EMC4 in each tissue had distinct effects depending on the age. These findings suggest a potential tissue-specific requirement for EMC4 in regulating reproductive capacity. To further investigate the role of EMC4, we assessed the lifespans of flies with tissue-specific EMC4 knockdown, aiming to determine if the lifespan data would support our fertility findings. Lifespan could offer further insights into the tissue-specific functions of EMC4 and its broader role in aging. Through examining the effects of EMC4 knockdown on lifespan, fertility, and fecundity in various tissues, our study illustrates the varied roles that EMC4 plays in organismal health and aging. Future studies will focus on investigating the molecular processes underlying EMC4's role in various tissues, including dissecting ovaries to observe egg chamber development and examining physiological differences in oogenesis.

The Principal of Charity: Do philosophical concepts such as the principle of charity and rationalization effect the likelihood that a person will change their mind?

Jinhua Adair ’26, Davis James-Rowe ’25, Dr. Paul Henne, Philosophy Department, Lake Forest College, Lake Forest IL 60045

More than ever, people have become fixed in their moral and political beliefs, making them increasingly resistant and unwilling to interact with arguments that challenge these beliefs. People evaluate opposing viewpoints unfairly and selectively endorse reasons and arguments that align with their beliefs, thus decreasing discussion and increasing polarization. Additionally, polarization may be linked to a larger antipathy and distaste for political opponents. This study aims to employ the philosophical concepts of the principle of charity and the rationalization principle to encourage people to view their opponents as rational agents who prioritize truth over winning an argument. The pilot study asked participants if they supported or opposed Universal Basic Income. After this, participants were shown reasons opposing their initial view. Before rating the quality of each reason, participants described the reason in their own words, from the point of view of someone who holds the opposing view, or to explain why a rational person would find that reason compelling. After doing this, participants rated the quality of the reasons and were given the opportunity to change their mind or keep their original position. No evidence was found to suggest that employing the rationalization principle affected people’s resistance to change. However, it was found that people who used the rationalization principle rated individual reasons higher than those who did not. Moving forward on this project, participants will be asked to come up with their own reasons for the opposing position rather than evaluating the reasons this study provided, to see if that will make them more likely to change their minds.

Gene Therapy Approaches for Inflammation Reduction with Applications in Alzheimer's Disease

Martha Alatorre ‘26, Mike Milovanovic, and Dr.Robert Marr, Department of Neuroscience, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60045

The consequences of inflammation in Alzheimer's disease are profound and have gained the attention of many. Its implications on neurodegeneration and cognitive decline call for new approaches. Gene delivery methods to target the NLRP3 inflammasome look to reduce AD pathology. The development of these gene therapeutic approaches require the construction and characterization of gene transfer vectors that inhibit inflammation. Our vectors are designed to deliver a secreted dominant negative inflammasome inhibitor, which could suppress the activation of the inflammasome in hopes of improving memory and cognitive function. Ideally, this inhibitor would be expressed in the periphery and cross into the brain allowing for easy administration and less invasiveness. We set out to set the NLRP3 inhibitory capacity of a gene transfer vector expressing a brain-penetrant form of an NLRP3 inhibitor.  Our in vitro assay utilized a human monocyte cell line stimulated with inflammatory agents. We found that our vectors tended toward inhibition of inflammation in these monocytes through suppression of interleukin 1-beta (IL-1b) expression. Future experiments will assess the in vivo brain penetrance of our approach and subsequent assessment of inflammatory pathology in mice.

The impact of pregnancy on mood, cognition, and microglia function in Alzheimer’s disease mice.

Perla Arias ’25 and Dr. Holly C. Hunsberger, Center for Neurodegenerative Disease and Therapeutics, Rosalind Franklin University of Medicine and Science

Alzheimer’s disease (AD) impacts six-million Americans, 2/3rds of whom are women. Women are more susceptible to developing AD due to a variety of social stress factors, differences in immune responses, and a decline in estrogen. Previous research has shown that pregnancy offers protective barriers to women, reducing the likelihood of developing dementia-like disorders. Notably, pregnancy has the ability to modify a woman’s inflammatory response. This interaction between pregnancy and inflammation is critical given that there is microglial upregulation to clear amyloid plaque burden in the brain. In some instances, the activation of microglia can promote the phagocytosis and clearance of those toxic proteins, but if microglia become overactivated, a surplus of inflammatory mediators are released. Here we aim to understand how pregnancy impacts cognition and microglia activation in Alzheimer’s disease mice. To answer these questions, we used behavior testing and immunohistochemistry to analyze cellular activity in the hippocampal region of male and female naive and postpartum mice. We found that 1) litter-bearing mice exhibit slight memory impairment with age and 2) litter size was indicative of memory impairment in AD mice. Interestingly, the sex of the pups also impacted affective behaviors. Furthermore, immunohistochemistry using microglia markers can give insights into the complexity of microglia function in naive and litter-bearing control or AD mice. Overall, this research provides a deeper understanding of how pregnancy influences brain pathology and AD symptoms.

The effects of repeated monaural transcutaneous auricular vagus nerve stimulation on pupil size during a working memory task

Hamzeh Arabiyat ‘27, Juliana Hougland, Dr. Shawn Flanagan, Flanagan’s Lab, Podiatry College of Medicine, Rosalind Franklin University of Medicine and Science

Transcutaneous auricular vagus nerve stimulation (taVNS) shows promise for enhancing cognitive function, potentially through activation of the locus coeruleus-norepinephrine (LC-NE) system. This study investigated the effects of daily monaural taVNS on pupillary responses and performance during the Sternberg Working Memory T ask (SWMT) in twelve healthy young adults. Participants received either active or sham taVNS for 10 consecutive days, with a two-week follow-up. Stimulation was administered throughout the SWMT while measuring binocular pupil size and task performance across three difficulty levels. Results showed that task difficulty was inversely related to accuracy and directly related to response time, with both metrics improving over time. Pupil size consistently increased during recall compared to memorization phases. Active taVNS was associated with greater pupillary dilation, independent of task difficulty or session number, suggesting enhanced LC-NE system activation. This effect showed no evidence of habituation with repeated daily exposure. These findings support the potential application of taVNS for cognitive enhancement and contribute to our understanding of non-invasive neuromodulation techniques.

Instructor Presence in Instructional Video: Student Recall, Perception, and Anxiety

Stephanie Arreola ‘27, Kiera McKee ‘27, and Nora McLean, Psychology Department, Lake Forest College, Lake Forest, IL 60045

Learning research and educational psychology have examined the effects of instructor presence in video lectures on learning (e.g., recall, transfer), attention distribution, and perception. Although instructor presence may not facilitate or compromise learning, it has been suggested that instructor presence may improve student perceptions in terms of their educational or learning experience, that the benefits of instructor presence may be dependent on difficulty of the content being delivered, or that learning and/or attention are only enhanced when instructor presence includes specific features, such as dynamic drawings or eye contact. In this study, we explored how instructor presence and lecture topics in asynchronous learning videos would affect recall, perception, and acute stress. We predicted that instructor presence in asynchronous lecture videos would lead to more positive perceptions of learning experience, and therefore lower acute stress after learning. Based on Cognitive Load Theory and the Cognitive-Affective-Social Theory of Learning in digital Environments (CASTLE) Theory, we predicted that instructor presence could either improve or hinder information recall. We randomly assigned lecture videos to student participants, alternating instructor presence (present vs. absent) as well as lecture content (statistics vs. stress psychology). We measured state anxiety levels before and after participants watched a lecture video, assessed learning retention through pre- and post-recall quizzes, and evaluated individual subjective perceptions of learning. We found no main effects of instructor presence on state anxiety or recall. However, students had higher post-recall scores for the psychology of stress content, and at post test, those who watched the statistics video had higher acute stress scores compared to those who watched the psychology of stress video. This study has relevant implications for exploring strategies to facilitate learning when designing virtual material, in order to better support students academically and emotionally.

Learning induces suppression and activation of neurons in different distinct areas of aplysia pedal ganglion

Arnav Bajpai ‘26, Viral Mistry, Dr. William N. Frost, Department of Cell Biology and Anatomy, Rosalind Franklin University of Medicine and Sciences, North Chicago, IL 60045

Aplysia californica is a sea slug that has been a crucial model organism for providing fundamental insights into the cellular basis of learning and memory. Our lab has previously shown that Aplysia's escape locomotion network consists of many rhythmically active efferent neurons located in spatial-functional clusters across the pedal ganglion, but how these neurons change as the motor program undergoes non-associative learning is still unknown. Using intracellular electrophysiology, we recorded from neurons in different regions of the pedal ganglion in an isolated CNS during a 5-trial non-associative learning protocol. We found distinct regional differences across learning. In Area B (superior-lateral area in between the cerebro-pedal and pedal-pedal commissure) we observed tonically active neurons at rest that were suppressed with repeated stimulation, while in area C & D (C being inferior-lateral proximal to pedal-pedal commissure and D being inferior-lateral proximal to p9), we observed neurons that fired rhythmically at rest and became more active with repeated stimulation. We also characterized various membrane properties of these regions, including changes to resting membrane potential, intrinsic excitability, as well as how they performed during the motor program. These geographic differences  suggest that learning induced changes to Aplysia's escape network are localized to specific neuronal clusters, which may be a fundamental principle of how neural networks reorganize during learning. Future work will continue to investigate how specific clusters are differentially modified by learning, and determine if these regional differences persist with age.

Sex-Specific Effects of Oxytocin Receptor Modulation in the BNST on Stress and Anxiety Behaviors in Rats

Margarida Carreira ‘26, Joanna Dabrowska, and Susan Olson, Department of Cellular and Molecular Pharmacology, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60045

The bed nucleus of the stria terminalis (BNST) plays a crucial role in regulating stress and anxiety, and oxytocin receptors (OTRs) have been implicated in these processes. However, how OTR-expressing neurons in the BNST regulate stress and anxiety in a sex-specific manner remains unclear. This study aimed to examine the differential effects of OTR modulation on neuronal activity in the BNST of male and female rats. Using Designer Receptors Activated Only by Designer Drugs (DREADDs) to modulate OTR-expressing neurons and immunohistochemistry to measure neuronal activation, we compared OTR expression between sexes. The results revealed no significant sex-specific differences in neuronal activation or OTR expression. Both male and female rats showed similar levels of OTR modulation in the BNST, indicating that OTR pathways may function similarly across sexes in the context of stress and anxiety regulation. Further research is needed to explore whether other factors, such as different stress paradigms, could uncover sex-specific effects.

Pathogenicity Assessment of Three Newer a-Synuclein Mutants Under Varying Expression Levels in Yeast Reveals Differential Toxicity

Kate Feist ‘27, Shanamon Chandavimol ‘27, Sebastian Gacek, Federica Bertolotti, Amanda Grassel, Carris Borland and Shubhik DebBurman, Neuroscience Program, Lake Forest College, IL 60045

Parkinson’s Disease (PD) is the second most common neurodegenerative disorder characterized by the death of midbrain dopaminergic neurons. This selective cell death is linked with the misfolding and accumulation of the protein, a-synuclein. Six a-synuclein mutants previously linked with early-onset familial PD (A30P, E46K, H50Q, G51D, A53T, A53E) are extensively well-studied for their mechanism of toxicity. In contrast, three newer a-synuclein mutants linked with familial and sporadic PD (A18T, A29S, and A53V) are less well-understood for their underlying toxicity mechanisms. We characterized these three mutants in a budding yeast ( S. cerevisiae) model and report that A18T, A29S, and A53V are all differentially toxic in yeast, with A53V being the most toxic, followed by A18T, and A29S. The level of mutant toxicity is correlated with a-synuclein aggregation, with A29S significantly less aggregated than the other two mutants. Each mutant’s toxicity is also expression-dependent: at lower concentrations, all three mutants become less toxic and equalize to each other’s level and lower than that of wildtype a-synuclein. These new mutants also reveal greater toxicity differentiation in several altered cellular/environmental conditions linked with PD: while all three are equally sensitive to altered SUMOylation, A18T and A53V are more sensitive to nitrative stress. We are currently evaluating whether the loss of the original amino acid (alanine) or the gain of the mutant amino acid (T, S, or V) is key to the toxicity of A18T, A29S, and A53V mutants. Specifically, the A53 position, we find more support for the gain of a new mutant rather than the loss of A, with toxicity linked with substitution mutants N, G, R, but not D. We are also testing the combinatorial impact of double mutants (A18T/A29S, A29S/A53V, A18T/A53V) and a triple mutant (A18T/A29S/A53V). Overall, our studies add new insight into the nature of toxicity of each of these rare mutants linked with PD.

Molecular Dynamics of Thyroid hormone Related Compounds - Insights for Deiodinases and Immune System Regulation in the Endometrium

Michael Chapa ‘26 and Mahmood Bilal and Svetlana Dambaeva, Clinal Immunology Lab, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60045

Thyroid hormones, primarily Thyroxine (T4) and Triiodothyronine (T3), are essential regulators of metabolism, growth, and reproductive health. Their production involves key enzymes that mediate the conjugation and organification of iodide, leading to the formation of T4 and T3. These hormones are further modulated by three deiodinase enzymes (DIO1, DIO2, DIO3), which can convert T4 to its active form, T3. Deiodinases are expressed at varying ratios in different tissues, including immune, liver, and endometrial cells, where they influence localized thyroid hormone activity. Dysregulation of this enzymatic machinery may contribute to reproductive disorders, though the specific mechanisms remain poorly understood. In this report, we investigate the role of deiodinases in women with Recurrent through molecular analyses. Utilizing sequencing, RT-PCR, we reveal differential expression of these enzymes between the two groups. Our data indicate that women with high DIO2 expression showed increased iodide transporter levels, while those with low DIO2 had elevated Natural Killer (NK) cell and immune markers, including NCAM1 (CD56), Perforin (PRF1), and Granzyme-B (GZMB). Interestingly, thyroid hormone receptor-beta (THRB) was more highly expressed in women with low DIO2 and DIO1 levels, suggesting possible differences in localized T3 activity. Finally, we observed that women with positive thyroid antibodies exhibited distinct patterns of thyroid hormone modulation compared to antibody-negative women. These findings provide new insights into the potential role of thyroid hormone regulation in reproductive failures.

The Genetic Component of Colon Cancer: Examining the STN1 Gene

Cadence Dempsey ’26, Department of Genetic Diseases and Department of Microbiology and Immunology, Rosalind Franklin University of Medicine and Sciences, North Chicago, IL 60054

Genetic alterations play a crucial role in the development and progression of cancer, with growing evidence highlighting the importance of telomere maintenance in genomic stability. The STN1 gene is critical for proper telomere replication, telomere protection, and maintaining genome stability. Mutations in STN1 lead to telomere shortening and chromosomal instability. We investigate the effects of a STN1 deletion in mice, specifically in colon tissue. We aim to understand the rate of colorectal cancer development and mortality that may result from the STN1 deletion. The goal of this research is to generate mice with different variations of functionality in the STN1 gene to observe the differences between mice with fully functioning STN1, those without STN1, and those with reduced STN1 expression.

Endoplasmic Reticulum Membrane Protein Complex (EMC): Distinct Roles of Individual Subunits

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

The endoplasmic reticulum (ER) is an organelle that plays a critical role in modifying, packaging, and inserting membrane proteins in the cell. The ER membrane protein complex (EMC), composed of 8-10 subunits, facilitates these processes. Malfunctions in several EMC subunits have been associated with a wide range of pathologies in humans, including neurodegenerative diseases, visual impairments, metabolic disorders, and certain cancers, such as gastric adenocarcinoma. Previous findings from our lab demonstrated that fruit flies ( Drosophila melanogaster) with a genetic reduction of EMC subunit 4 specifically in glial cells of the nervous system 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 there was something unique about the 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 resulted in normal development, lifespan, and locomotion, suggesting varying functional roles among EMC subunits. To further validate and explore these findings, future research should focus on measuring subunit levels in glial cells to better understand if the degree of reduction differs for each EMC subunit. Investigating the effects of subunit knockdown in other cell types apart from glia, such as neurons, and identifying specific proteins whose production is impacted by the EMC subunit reduction, would also be insightful. Our findings emphasize the importance of understanding the distinct roles of EMC subunits. Some subunits might be more dispensable for EMC function in certain contexts, such as membrane protein biogenesis, which is critical for nervous system function.

Event-related potential signatures associated with prosocial deception

Cecilia Flores ’25 and Dr. Naomi Wentworth, Department of Neuroscience, Lake Forest College, Lake Forest IL 60045

People lie every day, often for the benefit of others. These types of lies are referred to as prosocial lies. Emotional contexts frequently influence such lies, such as when a friend asks us to conceal their feelings of depression following a negative event. This study aims to identify the neural signatures associated with prosocial lying compared to truthful responses using electroencephalography (EEG).

During the experiment, participants will have their EEG activity recorded while engaging in a task organized into four blocks. In each block, they will view images of four different human faces, each displaying either an emotional (e.g., happy, sad) or neutral expression. Participants are assigned one face, designated as their "friend," and instructed that this individual has requested they hide their emotions from others. Consequently, when their friend appears in the task, participants must lie—indicating "emotional" when their friend's expression is neutral and "neutral" when it is emotional. For all other trials, they are required to respond truthfully.

We will analyze three event-related potential (ERP) components—P300, medial-frontal negativity (MFN), and late positive potential (LPP)—which represent short segments of EEG activity evoked by cognitive events. Previous studies on lie detection have identified significant differences in the amplitudes of these components when participants lie versus tell the truth. We hypothesize that notable differences in the amplitudes of these three components will also emerge when participants provide deceptive versus truthful responses regarding their friend's emotional state.

Inhibitory and Temperament in 3 and 5 year olds

Lucy Freeman ’25, Jia Zheng ’25,Ceci Flores ’25, Olivia Ramirez ’25, Alex Soto ‘27 and Dr. Naomi Wentworth, Psychology Department, Lake Forest, Lake Forest College, IL 60045

This study examines the interplay between inhibitory control and temperament in preschoolers (ages 3 and 5) to advance our understanding of early developmental dynamics. Inhibitory control, the cognitive ability to regulate impulsive responses, is critical for cognitive and socio-emotional development. Temperament embodies enduring aspects of one's personality and influences how one responds to the world by revealing biologically rooted patterns of emotion, attention, and motor responses. The study uses a multi-method approach, implementing the Flanker and Dinky Toys tasks to assess inhibitory control, and maternal report to measure temperament. The order of tasks is counterbalanced. The overall goal of the study is to examine the complex relationship between inhibitory control and temperament in preschool children. It is hypothesized that positive comments about temperament will be positively correlated with higher inhibitory control scores (H1) and that developmental differences between 3- and 5-year-olds will lead to significant differences in performance on inhibitory tasks (H2).

Genetic Influences on Post-Stroke Aphasia: Investigating Critical Neuroplastic Polymorphisms and Their Impact on Recovery

Md Farhan Fuad ’25, Kayla Beck, Jake Parsons, Isabel O’Malley-Krohn, Elizabeth Salley, Dr. Rick Lieber, Dr. Leora Cherney, Dr. Allen Heinemann, and Dr. Andy Domenighetti, Biologistics Lab, Shirley Ryan AbilityLab, Chicago IL 60611

Stroke remains a significant global health issue, often resulting in aphasia, a communication disorder that impairs language comprehension, expression, reading, and writing. Aphasia's impact on linguistic, cognitive-communicative, and quality of life outcomes for individuals is profound. Genetic factors, particularly the presence of single-nucleotide polymorphisms (SNPs) in neuroplasticity-related genes, have been suggested to influence both aphasia severity and recovery outcomes. This study investigates the relationship between aphasia severity in post-stroke patients and key SNPs, specifically within genes associated with brain function and repair, including APOE, COMT, BDNF, GFAP, and VEGF-A. Our research utilized DNA samples obtained from 249 participants who underwent standardized aphasia assessment using the Western Aphasia Battery-Revised (WAB-R). Genotyping of the SNPs was performed using Allelic Discrimination Assays. We examined the association between the initial severity of aphasia, as measured by WAB-R, and specific SNPs in APOE, COMT, and VEGF-A, while also considering BDNF and GFAP variants. Findings indicate that particular allelic variations in APOE, COMT, and VEGF-A may be associated with differing aphasia outcomes. For instance, certain APOE alleles were identified as potentially protective in homozygous forms, while specific alleles of COMT and VEGF-A were associated with increased severity. These results suggest a complex interplay between genetic polymorphisms and neuroplasticity, influencing post-stroke aphasia severity.In conclusion, this study highlights the potential of these SNPs to serve as biomarkers for aphasia prognosis, offering a foundation for future personalized therapeutic approaches. Further research is needed to elucidate the mechanisms through which these genetic variations impact neuroplasticity and recovery, ultimately enhancing clinical strategies to improve patient outcomes.

The Effects of circadian rhythms on the Expression of C-fos and  β-AdrR in the cortex

Sai Nikhita Gaddam ’26 and Dr. EunJung Hwang, Department of Cell Biology and Anatomy, Rosalind Franklin University of Medicine and Sciences, North Chicago, IL 60064

Circadian rhythms significantly influence physiological and neurological processes, yet the mechanisms by which they regulate neuronal activity remain underexplored. A previous study identified two genes in the motor cortex that are differentially expressed between mice handled during light and dark cycles: C-fos and beta-adrenergic receptors (β-AdrR). However, in that study, the dark-cycle mice were also water restricted, whereas the light-cycle mice were not, raising the possibility that water deprivation, rather than circadian rhythms, may have driven the observed gene expression differences. To disentangle these confounding effects, this study investigates the effects of light and dark cycles on the expression of the two key proteins: C-fos, an indicator of neuronal activation, and beta-adrenergic receptors (β-AdrR), which modulate neuronal activity via the norepinephrine system. We hypothesize that handling mice during the dark cycle will result in higher expression of both C-fos and β -AdrR in cortical neurons compared to handling during the light cycle. Ten mice were divided into two groups: one handled during the light cycle and the other during the dark cycle, with handling conducted over three consecutive days. Following the final handling session, mice brains were extracted, and immunohistochemistry (IHC) was performed to visualize and quantify protein expression. We successfully quantified protein expressions in the motor cortex in three pairs of mice. In two pairs, we observed higher expressions of both C-fos and β-AdrR in the dark-cycle mice, while the opposite pattern was found in the third pair. Therefore, we cannot conclusively determine that circadian rhythms are the underlying factor influencing the expression levels of C-fos and β-AdrR. Additional variables, such as handling-induced stress or other environmental factors, may also contribute to the observed variability. Further experiments, with a larger sample size are needed to isolate the specific impact of light-dark cycles on neuronal activity.

Characterization of the 5xFAD model for studying Alzheimer’s Disease

Nilufar Imomdodova ‘25, Dr. EunJung Hwang, Department of Cell Biology and Anatomy, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60045

Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by the accumulation of amyloid-beta (Aβ) plaques and the hyperphosphorylation of tau protein in neurofibrillary tangles, leading to progressive cognitive decline. AD is the leading cause of dementia worldwide, with an ever-growing socioeconomic burden. Despite its prevalence, the underlying mechanisms driving AD remain unclear. Various animal models have been developed to mimic the pathological features of AD, aiding in the development of potential therapeutic interventions.  In this study, I focus on the 5xFAD mouse model, which is genetically engineered to express five familial mutations that account for roughly 2% of all human AD cases. Although extensive literature highlights the advantages of the 5xFAD model in recapitulating key aspects of AD pathology, one major limitation is the incomplete characterization of the timeline for cognitive decline and its relation to the Aβ plaque accumulation.  The aim of this research is to evaluate cognitive function in 5xFAD mice using the International Brain Laboratory (IBL) task and to investigate its correlation with Aβ plaque deposition. The IBL task is designed to assess learning, memory, attention, and decision-making abilities—cognitive functions that are expected to deteriorate in 5xFAD mice due to neuronal loss. This approach provides a novel avenue for assessing complex cognitive decline in 5xFAD mice and contributes to a deeper understanding of AD progression. Preliminary findings from our study revealed no significant differences in IBL performance between 5xFAD and control mice, nor between male and female mice at 2, 5 and 7-8 months of age, despite pronounced plaque accumulation in 5-8 month-old mice, with more extensive accumulation in females. These results suggest a decoupling between cognitive decline and Aβ plaque formation, indicating that significant cognitive decline in 5xFAD mice may appear only after 9 months or older.

Investigating the correlation between financial leverage and biodiversity risk of the S&P 500 companies (2000 – 2020)

One Kenosi ’26, Astrid Castro, Judith Johnson, and Dr Linh Pham, Economics Department, Lake Forest College, Lake Forest, IL 60045

This study investigates the correlation between biodiversity risk and financial leverage in S&P 500 firms over two decades (2000-2020). With growing environmental concerns and the increasing emphasis on corporate social responsibility, our research aims to provide empirical evidence on how biodiversity disclosures impact firms’ financial outcomes. We collected data from firms’ 10-K statements, focusing on biodiversity-related disclosures, and analyzed their relationship with financial leverage, using leverage equations such as “total debt to book assets” and “total liability to book assets.” Control variables included firm size, profitability, tangibility, and price-to-book ratio, and we employed a fixed effect regression model to control for omitted variable bias. Our findings reveal a significant inverse relationship between biodiversity risk and financial leverage, indicating that firms with higher biodiversity risk experience reduced financial leverage, potentially due to lenders' hesitance to finance environmentally risky firms. This research underscores the importance of integrating environmental sustainability into corporate strategies, benefiting both global biodiversity efforts and firms' financial health. Future research could further explore the long-term effects of biodiversity disclosures and other environmental factors on corporate performance.

Synucleinopathies: Molecular Determinants of β-Synuclein and γ-Synuclein Toxicity in a Yeast Model

Holly Kiernan ‘26,Leslie Casares ’26, Federica Bertolotti, Shanamon Chandavimol, Tracey Nassuna, Ryan Ossselborn, Sebastian Gacek, Shubhik DebBurman

Synucleinopathies, a group of disorders characterized by the abnormal folding and aggregation of proteins from the synuclein family (including α-, β-, and γ-synuclein), encompass Parkinson’s Disease (PD), the second most prevalent neurodegenerative condition. While α-synuclein's role in PD is well-researched, 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), and γ-synuclein inclusions are linked with ALS pathology. At SfN2023, we reported that -synuclein are differentially toxic, whereas 𝛾-synuclein is non-toxic in our Saccharomyces cerevisiae (budding yeast) PD model system. Here, we further evaluated the toxicity potential of β- and γ-synuclein by looking at their toxicity, localization, and expression using yeast assays. We evaluated substitution mutants for disease- causing β-synuclein mutations V70M and P123H, by changing the original amino acid with a different hydrophobic residue (V70), and with other polar and basic residues (P123). We expressed mutants swapping known familial mutations in α- and β-synuclein onto each other (α-, β- and γ-synuclein). We report that: 1) Substitution mutants show evidence for the gain of polar and basic amino acid cause toxicity in P123H-β-synuclein mutant, while hydrophobicity is key for V70M-β-synuclein toxicity; 2) α-synuclein familial mutations when swapped into β-synuclein show that amino acids A18, A29, A30, E46, G51, and A53 can regulate β-synuclein toxicity; 3) however, γ-synuclein’s non-toxicity is unaltered when swapped with α-/β-, familial mutations at A18, A30, E46, and V70. This study highlights the usefulness of yeast models in better understanding β- and γ-synuclein pathogenicity in neurodegeneration.

Sustainable Eradication of Plant-Parasitic Nematodes and Weeds Using Energy-Efficient Microwave Technology

Bellise Kigozi Nakimuli ‘25, Dr. Paolo Maccarini, Ronald Speigal, Dima Shmidov, Department of Electrical and Computer Engineering, Duke University, Durham, NC 27708

This research project focuses on developing a sustainable and novel approach to eradicate plant-parasitic nematodes (PPN) using electromagnetic technology. Our method leverages electromagnetic pulses to inhibit weed growth and target the eggs and infectious juveniles of PPN, aiming to offer an energy-efficient alternative to traditional chemical and mechanical control methods. In collaboration with North Carolina State University (NCSU), we are advancing the next-generation prototype of this system, designed for practical application in sweet potato and tomato fields. The primary innovation, microwave heating, consists of an automated cart, reminiscent of a Roomba, which integrates optimally designed lensing antennas and a solid-state source. The microwave heating approach involves heating the soil to a temperature that effectively eliminates nematodes and has shown promise in preliminary trials on sweet potato plots. However, it requires significant energy input. To address the energy demands, we have embarked on an alternative method using electromagnetic pulses. This technique requires less energy compared to microwave heating and offers a targeted approach to disrupt the biological functioning of the PPNs, effectively eradicating them. The development and optimization of this method involved comprehensive Multiphysics modeling to ensure energy efficiency. This project therefore represents a significant step toward sustainable agricultural practices by providing a viable, energy-efficient alternative for weed and nematode management. Future work will focus on further refining the technology and scaling up field applications to broader agricultural contexts.

Inferring the Formation and Populations of AM CVn Binaries with POSYDON

Dean Kousiounelos ‘25, Seth Gossage, and Vicky Kalogera, Center for Interdisciplinary Exploration and Research in Astrophysics (CIERA) and Department of Physics and Astronomy, Northwestern University, 2145 Sheridan Road, Evanston, IL 60201, USA

AM (Canum Venaticorum) CVn binaries are crucial verification systems for the upcoming Laser Interferometer Space Antenna (LISA) mission as they emit gravitational waves at the mHz range (0.3 < f gr < 1 mHz) and emit electromagnetic radiation in the optical and X-ray bands. Using a Binary Population Synthesis (BPS) simulation, POSYDON, we present an up-to-date inference on the population and distribution of AM CVn type cataclysmic variables (CVs) in our galaxy to predict the abundance of low frequency gravitational wave signals emitted from these binaries during LISA’s first observing run. We seek to explain the various formation channels of these short period binaries and create a large, open source grid of binary MESA simulations with up-to-date convective overshoot parameters for low mass stars (0.8 < M i< 8 M ) at solar metallicity (Z=0.0142 dex) and an initial orbital period parameter range of (0.01 < P orb< 1000 days). With these findings we can refine the contribution of AM CVn binaries to the stochastic gravitational wave background (SGWB) and prepare for LISA’s first observation.

The role of vision and the lateral line system in the jumping behavior of silver hatchetfish

Jeremy Levin ‘26, Hridey Kapoor ‘25,  Anais Azevedo, Kyle Lassen, Alyssa Silva, Jia Zhang, and Margot A.B. Schwalbe , Biology Department, Lake Forest College 

Many species of fish are capable of leaping out of the water, but fewer are known to do so deliberately and repeatedly. Jumping behaviors in fish are likely controlled by multiple sensory systems, including vision and the mechanosensory lateral line, which help them evade predators or catch prey. In this study, we examined the distribution of the lateral line system in silver hatchetfish ( Gasteropelecus sp.) and their unique ballistic jumping behavior. We discovered that these fish possess an extensive lateral line system, particularly concentrated along the top of their skull and their deep, narrow ventral keel, using fluorescent microscopy. To provoke jumping, a custom device was used to deliver vibrational stimuli, and trials were captured on a high-speed camera under both light and dark conditions (with infrared light) and with and without a functional lateral line system. We developed a Hatchetfish-specific method to successfully ablate the lateral line system, as standard ablation methods proved ineffective (validated by fluorescence microscopy). Consistently, the fish reacted to the vibrational stimuli by propelling themselves out of the water with a single, forceful downstroke of their elongated pectoral fins. Variations in jumping behavior under different sensory conditions were observed and will be discussed, with future experiments exploring the potential involvement of other sensory systems in the jumping mechanics of silver hatchetfish.

Fitness effects of alternative resource allocation strategies in female bean beetles

Katina Lucas ’25, Lia Romanotto ’25, and Flavia Barbosa, Biology Department, Lake Forest College, Lake Forest, IL, 60045

Trade-offs are a central concept to life-history theory, arising due to differential trait investment within an organism. In the bean beetle Callosobruchus maculatus, larval density induces differential resource allocation into wings and gonads, and females reared under high densities also invest more in early-life egg production. Here we tested the hypothesis that early life oviposition is an adaptive life history strategy that emerges in response to density levels and environmental influences. We employed density manipulations in the egg and larval stages to generate individuals with different allocation strategies. Oviposition substrate was also manipulated to compare fitness effects in differing environments. We measured the effects of density and environmental influence in different female reproductive traits: lifespan, lifetime fitness and reproductive investment at different time points of the adult stage. Contrary to our hypothesis, females from all treatments had the same average lifespan and lifetime fitness, with females reared under both densities laying more eggs earlier in life and tapering off near the end regardless of environment. Females in a limited environment laid less eggs overall and laid more eggs than females in an unlimited environment when transferred from a limited to an unlimited environment.

Understanding the sex-specific effect of social isolation on Alzheimer’s disease mice

Jasmine Mendez ‘26, L. Toennies, H.C. Hunsberger, Lake Forest College, Center for Neurodegenerative Diseases & Therapeutics, Rosalind Franklin University of Medicine and Science, The Chicago Medical School.

Poor quality social environments have been shown to exacerbate age-related memory and neural dysfunction, particularly during the COVID-19 pandemic. However, the specific effects of social isolation on aging individuals remain poorly understood, especially regarding sex differences in cognitive decline and the incidence of Alzheimer’s disease (AD). This study aims to elucidate the sex-specific effects of social isolation on memory and social interaction in aging and AD mouse models. Our central hypothesis posits that social isolation differentially impacts long-term memory and social behavior in AD phenotypes across sexes. We will focus on the basolateral amygdala (BLA), hippocampus, and prefrontal cortex due to their sensitivity to social isolation and regulation of social behavior and memory. We will measure changes in excitatory (c-Fos) and inhibitory (PV) cell activation to determine whether there is an imbalance after isolation. Preliminary data indicate that acute isolation enhances context fear memory retention in female AD mice while impairing memory in males. Social interaction also declines after stress and isolation in females. To explore these findings, we will assess the impact of acute isolation on neuronal activation in control and AD mice of both sexes with cell counting will be performed by region to quantify parvalbumin (PV) and c-Fos expression. This approach will allow us to identify differences in regional neuronal activation based on experimental groups or observed behaviors. Our findings will provide insights into the neurobiological mechanisms underlying the effects of social isolation on aging and AD, contributing to a better understanding of how adverse social environments shape neural function and exacerbate cognitive decline across the lifespan.

CRISPLD2 Overexpression through pGEM-T Easy Cloning and Its Effect on cell-mediated Inflammation of Th17 cells in an in vitro pathogenic T-helper 17 (Th17) cell model

Minal Mohammed ’26, Joseph Reynolds, Kristen Patterson, and LP Adhikari, Center for Cancer Cell Biology, Immunology, and Infection, Rosalind Franklin University of Medicine and Science, North Chicago, IL, 60064, USA

Cysteine Rich Secretory Protein LCCL Domain Containing 2 (CRISPLD2) is a protein-coding gene that hinders the production of pro-inflammatory cytokines in monocytes and mice. It also plays a critical role in immune inflammation and regulation. This project studies the overexpression of CRISPLD2 in an in vitro pathogenic T-helper 17 (Th17) cell model, which allows us to determine its effect on Th17 cell polarization and effector function. The initial step of this protocol involves pGEM-T Easy cloning which includes placing a gene of interest, CRISPLD2, into a plasmid vector and replicating it in a host cell. The outcome of this technique was a successful replication of our gene of interest, and the process provided insight into the function of the gene in regulating T-cell activation and differentiation. We are interested in the overexpression of CRISPLD2 on interleukin-17A (IL-17A), which serves as a proinflammatory cytokine, in the hopes of hindering IL-17 expression in CD4 T cells and potentially improving Multiple Sclerosis (MS) symptoms. Multiple Sclerosis is an autoimmune disease that causes the degeneration of healthy myelin, impacting the central nervous system (CNS). This is due to the abundance of Th17 cells, which contribute to neuroinflammation. Although we cannot currently draw conclusions regarding CRISPLD2 and MS, further research will allow us to determine the possibility of therapeutic applications for MS patients. Currently, in vitro experiments are being conducted to assess the overexpression of CRISPLD2 on mice's spleen and lymph nodes. If evidence suggests that this gene could be relevant for T cell pathogenesis in MS, future directions include in vivo experiments through an Experimental Autoimmune Encephalomyelitis (EAE) mouse model to research the role CRISPLD2 on inflammation in MS patients.

Evaluating pleasantness, distinguishability, and directional associations of haptic stimuli in a mobility cane for blind/low vision users

Ellis K Mudrik ’27 and Frederick R Prete, Ph.D. Department of Biology, Lake Forest College, Lake Forest, IL 60045

Approximately 23 million blind/low-vision people use mobility canes. However, traditional canes cannot detect obstacles beyond their tip, necessitating collisions in lieu of avoidance. Our goal is to ameliorate this shortcoming by incorporating haptic (vibratory) feedback into the cane handle, triggered by tip-mounted distance sensors. These experiments were designed to improve that feedback. In Experiment 1, 33 subjects rated the ‘pleasantness’ and distinguishability of nine haptic stimuli (differing in frequency, duration and amplitude) generated by a DRV2605 haptic driver controlling a Precision Microdrives 306-10H ERM actuator housed in a prototype cane handle. Stimuli were combined into 20 unique triplets (groups of three) and presented randomly. Overall, triplet ratings were negatively correlated with stimulus frequencies (F (1,17)  > 10, p < 0.006), but not with duration. The eight triplets that met our criterion for pleasantness (mean rating > 3.7 on a five-point Likert scale) had lower median frequencies than less preferred triplets (88 vs 94 Hz, respectively; t  > 3.9, p < 0.0012). Of the nine individual stimuli, three of the four with the lowest amplitude occurred most frequently in the eight highest-rated triplets: “single soft fuzz,” “single strong pulse,” and “transition hum.” In Experiment 2, subjects indicated whether they associated individual stimuli with a direction (left, right, straight-ahead). Out of 468 claims of directionality, 43% were Straight-ahead, 30% were Left, 27% were Right. Although directionality claims were not randomly distributed across stimuli (ChiSq = 50.2, p = 0.0013), no individual direction/stimulus count reached significance. These results are consistent with our previous research and enhance our understanding of how to integrate haptics into assistive technologies.

The Impact of Thirst on C-Fos and Adrenergic Receptor Expression in the Motor Cortex of Mice

Lejla Murati ‘25, Dr. EunJung Hwang, Department of Cell Biology and Anatomy, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60045

Thirst is a powerful stimulus that induces physiological and behavioral changes in animals. Water restriction, which induces thirst, is commonly used in neuroscience research to motivate animals to perform and learn tasks. Water-restricted animals exhibit heightened arousal states, increased metabolic activity, and exploratory behaviors. They also show enhanced cortical activity, which likely reflects the neural state necessary for learning. However, the neural mechanisms linking thirst to this enhanced cortical activity remain unknown. A recent study found that cortical neurons in water-restricted mice show enhanced expression levels of immediate early genes (IEGs) and norepinephrine (NE) receptor genes, suggesting that thirst-driven enhanced cortical activity may be mediated by norepinephrine pathways. However, in that study, all water-restricted mice were handled during the dark cycle (active phase) of circadian rhythms, whereas control mice were handled during the light cycle. This raises the question of whether the enhanced expression of IEGs and NE receptor genes results from water restriction or circadian rhythms. In this study, we aimed to determine the role of water restriction in the expression of IEGs and NE receptor genes. We specifically focused on Beta-2 adrenergic receptors (as an NE receptor) and C-Fos (as an IEG). We hypothesized that thirst would increase the expression of Beta-2 adrenergic receptors and C-Fos. To test this, ten mice were divided into two groups: a water-restricted group (1 mL/day of water) and a full-water group (unlimited access to water). Each water-restricted mouse was paired with a full-water counterpart, forming five sets of two mice. Each set of mice was handled for five minutes at a fixed time for three consecutive days. On the third day, both mice in the set were perfused 45 minutes after handling to allow for C-Fos protein expression. Brains were extracted and fixed in paraformaldehyde. Double-antibody immunohistochemistry was performed to visualize Beta-2 receptors and C-Fos expression. Stained tissues were imaged using a Leica fluorescence microscope, and ImageJ was used to quantify the protein expression levels in the motor cortex. We successfully collected motor cortical tissue samples from the three sets of mice. In two sets, we observed greater expression of C-Fos and Beta-2 receptors in the water-restriction group compared to the full-water group, while this third set showed the opposite pattern. Although the current results are inconclusive due to the small sample size, we have established reliable methods for this experiment. We plan to collect additional samples in future studies to draw clearer conclusions.

Telomerase Levels Dramatically Increase in Ascospores

Dawid Oleksy ’25, Meklit Yimenu, Petra Urgacova’25 and Karen Kirk, Biology Department, Lake Forest College, Lake Forest IL 60045

Telomeres are repetitive noncoding sequences at the ends of chromosome that prevent DNA loss during replication. The primary enzyme responsible for telomere replication is telomerase, a ribonucleoprotein with two essential components, TER and TERT. TER provides the RNA template for telomere repeat synthesis, while TERT functions as a reverse transcriptase. Assembly of the two components occurs in the cytoplasm in Saccharomyces cerevisiae and in the nucleus in mammalian cells. The structure of TER in the filamentous fungus Aspergillus nidulans is partially conserved in both S. cerevisiae and mammalian cells but whether TER migrates to the cytoplasm or remains in the nucleus during telomerase assembly was unknown. We used the heterokaryon rescue technique in A. nidulans hyphae and found that TER remains in the nucleus and, thus, telomerase assembly occurs there. To further investigate this observation, we wanted to explore the expression levels of the TER and TERT genes at various stages of the life cycle. Nearly ten replications of RT-qPCR were used to determine expression levels in muti-nucleate hyphae, asexual conidiospores, sexual ascospores, germinating conidiospores, and germinating ascospores. Surprisingly, we found that the relative expression levels of TER and TERT were at least two-fold higher in the germinating ascospores compared to hyphae, even though PCR showed that the telomere lengths were similar. We also looked at expression levels in nkuA and POT1 mutant cells. We used these cells because nkuA and POT1 are involved in nonhomologous end joining and telomere protection, respectively, and because we wanted to test whether these mutations affected expression levels in the different cell types. The relative expression levels of TER and TERT were also higher in the germinating ascospores in these mutant cells. Hence, TER and TERT have higher expression in ascospores in both wild-type and mutant A. nidulans cells. These results imply not only the upregulation of TER and TERT, but possibly longer telomeres in sexual spores. A potential avenue for a future study would be the use of exon-exon junction primers during RT-qPCR. These primers would target the junctions between exons and ensure that only mature, spliced mRNA transcripts of TER and TERT are amplified. The use of exon-exon junction primers could help eliminate the detection of genomic DNA, thus providing a more accurate measure of active gene expression. This would be particularly valuable when analyzing expression levels in different stages of the life cycle, as it would allow for a clearer distinction between fully processed mRNA transcripts and any possible contamination or immature RNA

Effects of Simulated Menthol Cigarettes Ban on the Health Perceptions of Smoking: A Preliminary Analysis

Aaron Oster ‘26 and Nancy C. Jao, Department of Psychology, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064

In 2009, the FDA banned all characterizing flavorings in combustible cigarettes except menthol. Menthol flavoring in cigarettes has been shown to make it easier to smoke, increase nicotine dependence, and decrease an individual's ability to quit smoking. While the overall prevalence of cigarette smoking has decreased in the general population, the proportion of menthol cigarette (MC) use has increased among individuals who smoke cigarettes. Basic science research has suggested that MCs may pose more significant risks to cardiovascular health compared to non-menthol cigarettes (NMC), however, it is unknown if we see this in humans. The current study used descriptive analyses to examine preliminary data (N=5) from an ongoing clinical trial study to understand potential changes in perceptions of health risks and cigarettes smoked per day as individuals switch from smoking MCs to NMCs across five weeks during a simulated menthol cigarette ban. Results showed that participants reported increased perceptions of risk of smoking NMCs for both cardiovascular and lung diseases. From the figures, participants reported no change in perceptions of risk of smoking MCs for cardiovascular or lung diseases, even after switching to NMC use. Participants also reported an increase in the number of cigarettes smoked per day after switching to NMC use. Overall, preliminary findings suggest that switching from MCs to NMCs may impact smokers' awareness of the health risks associated with smoking, especially for NMCs. Future research will continue to provide insights for tobacco regulations on how a ban on menthol flavoring in cigarettes may affect health and behavioral outcomes in individuals who smoke MCs.

Observing Dopaminergic Neurodegeneration in a Caenorhabditis elegans Model of Parkinson’s Disease

Anjani Padhiar ’26 and Hongkyun Kim, Department of Cell Biology and Anatomy, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60065

Parkinson’s disease (PD) is a neurodegenerative disease that has several genes associated to its onset. Extensive research has identified genes that either directly cause PD or are associated with PD. One of the critical issues of this disease is not everyone who has a PD-associated gene will develop PD. Therefore, there could be an external factor, or a separate gene, that activates these PD associated genes and initiates neurodegeneration. The purpose of this study was to examine a Caenorhabditis elegans homolog ( lrk-1) of the most common PD-mutated gene in humans, LRRK2, and determine whether there was increased dopaminergic neurodegeneration when mitochondrial stress is increased. To understand the interplay between lrk-1 and mitochondrial stress response, we utilized a gain-of-function lrk-1 mutation, lrk-1GS, and a gain-of-function atfs-1 mutation, atfs-1(gf). ATFS-1 is a transcription factor that induces mitochondrial stress response. Specifically, we determined whether there was a significant difference between the neurodegeneration of the control and the strain with only lrk-1GS, as well as a difference between the strain with only atfs-1(gf) and the strain with both genes ( lrk-1GS;atfs-1(gf)). We observed four strains of C. elegans (control, lrk-1GS, atfs-1(gf), and lrk-1GS;atfs-1(gf)) on day 1 and day 2 of them being adults; all worms expressed a GFP transgene in dopaminergic neurons.  Images of their anterior dopaminergic neurons and dendrites were collected through an inverted fluorescence microscope. Data of neurodegeneration was collected through counting the number of blebs on all their dendrites. We found that there was no significant differences in blebbing between the control and the lrk-1GS strain, nor the atfs-1(gf) and lrk-1GS;atfs-1(gf) strains for both day 1 and day 2. Although there was no significant difference between the latter on the 2nd day, it was approaching significance. Overall, this was the beginning stage of research between this homolog of LRRK2 and atfs-1(gf) to obtain initial data.

Insights into the Function of Mtb-BrkB via Copurified Protein Partners with M. Smegmatis

Piotr Pawlowicz ‘25, Will Conrad Department of Biochemistry and Molecular Biology

Lake Forest College, Lake Forest, IL, 60045

Tuberculosis (TB) is a respiratory disease caused by the bacterium Mycobacterium tuberculosis. According to the World Health Organization (WHO), in 2022 10.6 million people fell ill with TB and of those, 1.3 million passed away from TB complications. While antibiotics for treatment are available, those with drug sensitive TB must take multiple antibiotics for a prolonged amount of time (6 months). In addition, TB has shown to have an increasing number of variants that are resistant to multiple antibiotics (MDR-TB), making it more difficult to obtain treatment, as those with MDR-TB typically must take more antibiotics for a longer time (Usually 18 months, can be longer.) As such, research in TB has shifted toward finding new drug targets to create more effective treatments and to reduce the treatment time for TB. One such drug target is the novel protein Rv2707, an ortholog of the gene Bordetella resistance to compliment killing gene B (BrkB). In prior research, Rv2707 (Mtb-BrkB) mutation has shown attenuation of extracellular and intramacrophage growth in a in vivo model using zebrafish. These results have big implications as this is the first known instance of a mycobacterial virulence factor with an extracellular growth defect in vivo. The goal of this project is to determine the function of Mtb-BrkB; this will be done in three steps. The first step is to use the model organism Mycobacterium smegmatis to express the Mtb-BrkB ortholog, MSMEG_2755, and then purify it. Once purification is complete, the second step is to use Protein/Peptide Mass Spectroscopy to analyze our purified protein to determine if there are any binding partners to MSMEG_2755 The final step is to analyze the P/P-MS data and to identify the most likely binding partners to MSMEG_2755 and use them to provide clues to the true function of Mtb-BrkB. Here, we show successful expression and purification of Mtb-BrkB in both smaller and larger volumes in M. smegmatis. We also show successful P/P-MS of Mtb-BrkB along with a negative control Mtb-pGE167. Finally, we also show initial results of potential Mtb-BrkB binding partners.

Quantification of Microglia in the Hippocampus and Cortex of a Ts65Dn Mouse Model

Ekaterine Priovolos ’26 and Beth Stutzmann, Center for Neurodegenerative Disease and Therapeutics, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60045

Down syndrome (DS) is a genetic condition caused by a partial or extra copy of chromosome 21. This extra copy leads to amyloid precursor protein (APP) gene overexpression, which is responsible for forming amyloid plaques observed in Alzheimer's disease (AD). Typically, microglia found in the central nervous system aid in immune responses, maintain neuronal health and respond to injury. However, while microglia may aid in the clearance of amyloid plaques, the upregulation and overactivation of microglia lead to a catastrophic, proinflammatory state that furthers the neurodegeneration already occurring. Here, we used immunohistochemistry to quantify microglia in the cortex and hippocampus, particularly CA1 and dentate gyrus regions, of the Ts65Dn mouse model, a well-established model for studying Down syndrome. Specifically, we hypothesized that microglia density would increase in the Down syndrome model compared to non-Ts65Dn mice due to the overactive immune responses and increased APP levels in DS. Additionally, we investigated the effects of maternal choline supplementation, which is thought to reduce autoimmune responses, improve cognition, and delay age-related memory deficits in their offspring. In our preliminary data, we found marginally significant or strongly trending increases in microglia density in the dentate gyrus and cortex from Ts65Dn mice relative to the nonDS controls, and the choline-exposed mouse groups (DS and nonDS). Even though the exact role of microglia and their mechanisms are still unclear, it is evident that they play a crucial function in determining the level of neurodegeneration that occurs in Alzheimer's disease and Down syndrome. Importantly, maternal choline supplementation appears to offer therapeutic effects in calming brain neuroinflammatory responses. Understanding the position of microglia can potentially provide a fresh way of combating these devastating disorders.

The Impact of VCD-induced Early Menopause on Alzheimer's Disease Mice

Trisyia Rahimi ‘26, and Holly Hunsberger, Center for Neurodegenerative Diseases & Therapeutics, Rosalind Franklin University of Medicine and Science, IL 60045

Alzheimer’s Disease (AD) is a debilitating neurodegenerative disease marked by gradual memory loss, behavior changes and neuropsychiatric symptoms like depression and anxiety. 2/3 of those impacted by AD are women whose symptoms develop at faster rates compared to men. Although the influence of biological sex on AD are unclear, preliminary research suggests that the depletion of neuroprotective hormones like such as estrogen contribute to the progression of cognitive decline. Perimenopause is the period 4-8 years before the onset of menopause, coinciding with the prodromal period of AD, characterized by the appearance of its pathological hallmarks, namely tau tangles and amyloid plaques. With the administration of 4- vinylcyclohexene diepoxide (VCD) injections to control and Alzheimer’s mouse models, menopausal transition more naturally mimics that of humans in comparison to surgically induced menopause through ovariohysterectomy (OVX). This method allows for the ability to compare the irregular ovarian hormone fluctuations characterized by perimenopause and cognitive decline seen in AD. The mice performed a behavioral testing paradigm concurrently with estrous cycle tracking to further understand the relationship between behaviors exhibited in the tasks with the stage of estrous. Repetition of the testing paradigm, coupled with obtaining cytology to track estrous cycles, allows for an observation of the impact on ovarian hormone changes on AD pathology.

The effects of male antennation behavior on female mating preference in bean beetles

Lia Romanotto ’25, Sylvie Paddon-Jones ’25, and Flavia Barbosa, Biology Department, Lake Forest College, Lake Forest, IL, 60045

Antennation is an observable courtship behavior in bean beetles during in which the male rapidly taps the female’s abdomen with his antennae prior to copulation. Previous research shows that changes in the frequency of antennation may influence female bean beetle’s willingness to copulate. In this experiment, we evaluate female mating preferences for the intensity of the antennation behavior of a courting male by testing the hypothesis that female bean beetles have a preference for antennation behavior. We manipulated antennation by ablating the left antenna of males, and allow females to mate twice, with a manipulated and an intact male. We then measured female preference through latency to copulate and latency to kick. We predicted that females will be less responsive to mating attempts from male beetles with manipulated antennae. This experiment aims to provide an understanding of the importance of antennation rate in female mate choice, in a species where courtship has not been considered an important factor in sexual selection.

Synthesis on Anti-Microbial Natural Products (Chaetoxanthone D)

Alexander Seeyavosh Shanov’25, Haris Zukancic’25, Sona Akiyama’27 and Dr. Paul Gladen, Department of Chemistry, Lake Forest College, Lake Forest, IL, 60045

Xanthones are tricyclic compounds with diverse biological activities including anticancer, antidiabetic, and antimalarial activity. Our research focused on synthesizing Chaetoxanthone D starting from inexpensive, commercially available materials. We explored a scandium triflate catalyzed coupling reaction with a variety of starting xanthones as our key transformation, leading to the successful total synthesis of Chaetoxanthone D. Future efforts will be focused on optimizing the reaction parameters for the scandium triflate catalyzed coupling and the purification conditions for this reaction. Successfully synthesizing pure Chaetoxanthone D will enable biological analysis and aid in developing new antiprotozoal treatments with fewer side effects from naturally derived products.

Draining the Social Battery: Investigating Neural Mechanisms of Altered Social Motivation Following Brief Social Satiation and Deprivation in Rodents

Michelle G. Soriano ’25 and J. Amiel Rosenkranz, Department of Cellular and Molecular Pharmacology, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60045

Social behaviors are an important marker for normal brain development in children and young adults. Several psychiatric disorders are characterized by their negative effects on social behaviors, such as autism spectrum disorder and schizophrenia. Social interactions are inherently rewarding, and any changes to social motivation may reflect alterations in how the brain encodes the value of social interactions. The basolateral amygdala (BLA) is an area of the brain that communicates with several regions to encode the value of stimuli that predict rewards. The exact mechanism of how the BLA can influence social motivation is not well understood, but the anterior cingulate cortex (ACC) has been documented to have an age-dependent role in driving or suppressing BLA activity. The purpose of the present study was to (1) investigate the effect of brief changes to the social environment on the neural activity of rodents, (2) determine if ACC-BLA circuitry is driving these changes, and (3) to identify possible sex-dependent changes.

Young adult male and female Sprague–Dawley rats (male n = 29, female n = 33) were randomly assigned to one of three experimental housing conditions: social deprivation (1 rat/cage), social satiation (4 rats/cage), or control housing (2 rats/cage). To identify BLA inputs, 18 of those rats (male n=9, female = 9) were given intracranial injections into the BLA with (AAVrg-hSyn-Cre-P2A-dTomato) retrograde virus. To assess differences in social motivation, 24-48 hours after altering their social environment, behavior assays were conducted (social preference test, open field social interaction session). Preliminary results from two-way ANOVAs on the social preference test show that rats spent significantly more time investigating the novel rat zone compared to the novel object zone. However, no significant differences were observed between the social deprivation, satiation groups, or control groups. Further analysis, including other measures of social function and immunohistochemistry analysis for activation and inactivation, is ongoing to refine these results and explore potential interactions between experimental conditions.

Identifying the Kaposi’s Sarcoma-associated Herpesvirus (KSHV) Latency Protein involved in the Induction of the Water Channel Protein Aquaporin-3 (AQP3)

Nabah Sultan ’25, Christopher Kywe, and Dr. Neelam Sharma-Walia, Department of Microbiology & Immunology and Cancer Cell Biology, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60045

Kaposi’s Sarcoma-associated Herpesvirus (KSHV or HHV-8) can cause two types of cancer: Kaposi's Sarcoma (KS), a skin cancer, and Primary Effusion Lymphoma (PEL), a B-cell cancer. The virus can remain dormant in the tumor cell, become active, and replicate when the immune system is weakened. Specific segments of viral gene expression, known as "open-reading frames," help us monitor the virus's cycle and progression. Latent KSHV DNA is associated with the expression of several genes and microRNAs, including ORF73 (LANA-1), ORF72 (v-cyclin), K13 (v-FLIP), and K12 (Kaposin A). Sharma-Walia's Lab discovered that PEL cells infected with KSHV have higher expression of the Aquaporin-3 (AQP3) gene and protein levels compared to uninfected cells. AQP3 is a protein that facilitates the transport of water, glycerol, and hydrogen peroxide. It is involved in various cellular functions, ROS-mediated signaling, microbial pathogenesis, and inflammation-related responses, making it a potential target for therapy. This study aimed to identify which KSHV latency protein triggers the expression of AQP3. 293-cells were transduced with the control lentivirus vector PSIN or lentiviruses expressing ORF71 (vFLIP), ORF72 (v-Cyclin), ORF73 (latency-associated nuclear antigen; LANA-1), and K12 (Kaposin A) for 72 hours. We used quantitative real-time PCR (qPCR) and Western blotting to identify which latent KSHV ORF induces the water channel AQP3. The overexpression of ORF71 (vFLIP) led to AQP3 expression in 293-cells. Our results demonstrate that KSHV uses its latency proteins to hijack the host water channel protein AQP3, likely for its survival or other functions that benefit KSHV's ability to hide within the infected host cell. Further evaluation of these pathways in future studies will be significant.

Exploring Brain Waves Through ERP Analytics: Inhibitory Control, Conflict Monitoring, and Deception

Liam Thumser ’27, Rin Kato ’27, Ceci Flores ’25, and Dr. Naomi Wentworth, Psychology Department, Lake Forest College, Lake Forest IL 60045

In psychology, researchers have developed electrophysiological measures as a system of researching cognitive function. The goal of this research project was to explore the use of electroencephalography (EEG) by reviewing the existing literature on Electrophysiology and by practicing with BIOPAC EEG equipment. We investigated current methodology of how EEG data can be used to study different cognitive processes, such as bilingualism, inhibitory control, conflict monitoring, and lying/deception. We also investigated the different types of event related potential (ERP) components (the Pa, P3b, N2, and others) detected in EEG data when participants perform cognitive tasks. This literature review created key insights into how brain activity relates to attention, distraction, and cognitive control, with a purpose to create foundation for future research. The work contributes to a senior thesis aimed at further investigating ERP components elicited when one lies for prosocial reasons.

Synthesis and Characterization of Rare-Earth Stoichiometric Solids for Quantum Information Systems

Amy Tram, Jack A. D’Amelio, Daniel P. Shoemaker, Materials Research Science and Engineering Center, University of Illinois, Urbana, IL, 61801

Rare earth stoichiometric solids are candidates for quantum information storage because their 4f electrons are shielded from the environment, a quality important for sensitive quantum systems. Europium materials are promising due to the clean 7F 05D 0 energy transition of europium(3+) ions. NaEu(IO 3) 4 crystals were determined to be more homogeneous than Eu(IO 3) 3, therefore they are the target for this project. Progress on hydrothermal synthesis parameters for NaEu(IO 3) 4 crystals are reported. Synthesis of the crystals was inconsistent, both NaEu(IO 3) 4 and Eu(IO 3) 3 were produced using factors expected to produce NaEu(IO 3) 4. Experimental parameters focus on the stoichiometry of reagents, mass scale of reagents, pH of the solvent, surfactant, and filtering versus not filtering the initial Eu(IO 3) 3 precipitate.

Exploring Brain Waves Through ERP Analytics: Inhibitory Control, Conflict Monitoring, and Deception

Liam Thumser ’27, Rin Kato ’27, Ceci Flores ’25, and Dr. Naomi Wentworth, Psychology Department, Lake Forest College, Lake Forest IL 60045

In psychology, researchers have developed electrophysiological measures as a system of researching cognitive function. The goal of this research project was to explore the use of electroencephalography (EEG) by reviewing the existing literature on Electrophysiology and by practicing with BIOPAC EEG equipment. We investigated current methodology of how EEG data can be used to study different cognitive processes, such as bilingualism, inhibitory control, conflict monitoring, and lying/deception. We also investigated the different types of event related potential (ERP) components (the Pa, P3b, N2, and others) detected in EEG data when participants perform cognitive tasks. This literature review created key insights into how brain activity relates to attention, distraction, and cognitive control, with a purpose to create foundation for future research. The work contributes to a senior thesis aimed at further investigating ERP components elicited when one lies for prosocial reasons.

Analyzing Murine Hepatitis Virus Type 1 (MHV-1) to model pathology of severe acute respiratory syndrome (SARS) in humans

Jakob Wepman ’25, Dr. David Everly, Department of Microbiology & Immunology, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60045

The study of respiratory infections has been of great concern since the COVID-19 (SARS-Cov2) pandemic.  While there have been advancements in preventative medicine of numerous viral respiratory infections, their adaptive nature consequently creates challenges in finding updated treatments for the mutated agents.  Using animal and in vitro models to simulate infection, we can continue to identify cellular pathways induced by these pathogens, one of interest being Extracellular signal-related kinase (ERK).  Intranasal mouse hepatitis virus type 1 (MHV-1) is a beta-corona virus that induces pneumonia in mice, which is analogous to pulmonary disease consequential of severe acute respiratory syndrome coronavirus (SARS-Cov) in humans.  Due to their similarity, MHV-1 is an ideal animal model to conduct in vitro analysis.  This experiment aims to grow and quantify viral titers of MHV-1, followed by measuring the prevalence of P-ERK and t-ERK protein products via florescent western blot analysis.  The first four weeks of the summer included passaging L2 cells until there were enough cells to work with.  The proceeding five weeks involved growing a P1 and P2 stock of MHV-1 via plaque assays using L2 cells.  After having a quantified P2 stock of MHV-1 from the initial P1 stock, the final three weeks of the experiment involved running a fluorescent western blot of the P2-infected cell lysate samples collected.  Each P2 MHV-1 infected sample was incubated at different intervals before lysates were collected: 48h, 24h, and 12h.  Once the gel was run, we treated the membrane with beta-actin (control), P-ERK antibodies, and t-ERK antibodies.  It was concluded that the ERK pathway is relevant in MHV-1 pathology, as there were distinct bands on the western blot suggesting that the antibodies for ERK bound to the proteins on the membrane.  Overall, using animal models to study the cellular mechanism of infectious agents, such as MHV-1, can provide further insight into potential treatments for similar diseases in humans.