Neuroscience

Kevin Le, kle23@earlham.edu
Earlham College, with Dr. Molly Gallop

Fat Percentage Diets Impact on Mice Health
Obesity has been on a steady rise with over-processed food infiltrating everyday life. Society has conflated weight to be the prime indicator of health with new diets coming out every few months to be the quick fix for people's weight problems. A diet that hasbecome popular in recent years is the ketogenic diet, or a diet that has low to no carbs and contains high fat. As a new trendy diet,not many studies have been published about the health impacts of the high-fat low-carb diet. This study intends to produce empirical results on the health and fitness impact of 90 C57Bl/6J female mice that have undergone different fat percentage diets (10%-90%). What we found was the mice with the higher fat percentage diets had higher cholesterol levels and had high triglyceride counts when fasted (90% fat). Body weight also increased as dietary fat increased (10%-60%). This study highlights the importance of dietary research into newer 'fad' diets as they may come with unexpected health impacts. 
 

Valeria Muniz, valeria_muniz1@baylor.edu
Baylor University, with Dr. Elisabeth G. Vichaya

Investigating the effects of voluntary exercise on cisplatin-induced cognitive impairment in an APOE4 murine model
Chemotherapy-induced cognitive impairment (CICI) affects up to 78% of cancer survivors, often impacting their quality of life long after completion of chemotherapy treatments. Symptoms of CICI include cognitive and memory deficits, executive dysfunction, and problem-solving difficulties. There are no FDA-approved treatments to alleviate CICI. While the underlying mechanisms remain unclear, reductions in neurotrophic factors, including BDNF, have been implicated. It has been reported that voluntary wheel running in mice can rescue cisplatin-induced dysregulated BDNF. In a recent study from our lab, we demonstrated that cisplatin induces cognitive deficits in mice and that mice carrying the ε4 allele of the apolipoprotein E (APOE4) are at increased risk for cisplatin-induced BDNF dysregulation within the frontal cortex. Therefore, within the current study we are investigating if voluntary exercise can mitigate cisplatin-induced cognitive impairment and BDNF in APOE4 mice. The puzzle box and novel object/placement recognition tasks were used to evaluate cognitive impairment, and the frontal cortex and hippocampus will be analyzed for alterations within BDNF and related neurotrophic pathways. Behavioral and tissue analysis are ongoing. Understanding the relationship between neurotrophic signaling and cisplatin-induced cognitive impairment in an APOE4 genotypic murine model can help broaden insight into risk factors, mechanisms, and potential treatments for CICI. 

Jada Bostick, jeb1422@mavs.uta.edu
University of Texas Arlington, with Dr. Qing Tang

Exploring hyperinflammation involved in Staphylococcus aureus small-colony variants and the host using CRISPR-Cas9 knockout approaches
Cystic fibrosis (CF) is a genetic disorder caused by mutations in the CFTR gene, leading to thick mucus buildup, impaired mucociliary clearance, and chronic lung infections. Persistent colonization by pathogens such as Staphylococcus aureus and Pseudomonas aeruginosa, particularly in multidrug-resistant forms, contributes significantly to pulmonary decline. Thymidine-dependent small-colony variants (TD-SCVs) of S. aureus are especially problematic due to their resistance to antibiotics and their ability to survive in the biofilm-rich CF lung environment. TD-SCVs provoke heightened inflammation, partly through activation of the STING pathway, but additional mechanisms remain unclear. Our lab has identified CCL3 as a key chemokine upregulated during TD-SCV infection, which recruits neutrophils and drives inflammation. Evidence suggests this may occur through the MyD88 pathway, possibly initiated by Toll-like receptor 2 (TLR2), which is highly expressed on macrophages in CF lungs. We hypothesize that TLR2 is a critical upstream regulator of CCL3 expression during TD-SCV infection. To investigate this, we will perform TLR2 knockout studies in macrophage models to clarify its role in the inflammatory cascade. These findings may reveal therapeutic targets to reduce chronic inflammation and preserve lung function in CF patients.