The current literature using the Activity Based Anorexia (ABA) animal model as a method of studying human Anorexia Nervosa (AN) has produced inconsistent results when attempting to study the differences in developing this disorder based on biological sex. As a result, these studies have not determined the underlying neural mechanisms of these inconsistencies. Past research shows that a subpopulation of neurons within two subregions of the central extended amygdala (EAc) exhibit traits of sexual dimorphism and are necessary for the development of ABA. Using Designer Receptors Exclusively Activated by Designer Drugs (DREADD) technology, we were able to add and individually target the hM3Dq receptor within these two subregions necessary for ABA development. The activation of these regions is expected to disrupt the levels of sex hormones causing changes in the estrous cycle, thus identifying the central extended amygdala as a potential region of interest for sex differences in ABA. This study tests this concept by measuring the effect of activating these neurons on sex hormones in 14 mice through estrous cycle testing. This study resulted in no discernible connection between the activation of the neurons within the two subregions in the EAc individually and estrous cycle changes. Based on these results and research by Schnapp et al. (2024), a future study focusing on simultaneous activation of the two subregions in the EAc may provide insight into the sex differences in ABA development.

The discovery of the glymphatic system about a decade ago has revolutionized our understanding of the metabolic waste removal process in the brain. The glymphatic system involves flow of cerebrospinal fluid (CSF, a colorless fluid composed primarily of water) through the brain to remove waste molecules. Rapidly growing research on the glymphatic system continues to reveal how its dysfunction plays an important role in neurodegenerative diseases such as Alzheimer’s disease. However, the driving mechanism of the glymphatic system is still poorly understood because of the complexity of performing in vivo quantitative measurements to accurately characterize CSF flow. This study employs surgical methods and two-photon microscopy to collect in vivo videos of fluorescent microspheres flowing in CSF. Data analysis is conducted by performing particle tracking velocimetry to compare mean particle flow speeds between mice of different ages. Prior studies demonstrate that glymphatic transport decreases with age, but our preliminary results suggest there is no significant difference in mean flow speed between young and old mice. Our research provides valuable insights for conducting more experiments on old mice and quantifying the CSF flow at the surface of the brain.

The Tau protein is a microtubule-associated protein responsible for stabilizing the structure of cells. It is well known that the malfunction of these proteins causes them to aggregate, forming clumps. This malfunction is highly correlated to cell death and neurodegeneration associated with diseases such as Alzheimer's. While it is known that there is a deep correlation between tau aggregation and these diseases, the underlying biochemical mechanisms are not well understood. This lab aims to better understand the role of Tau in neurodegeneration by creating a pathological model in rats. Using a Viral Gene delivery technique, a human Tau gene was injected into the hippocampi of 6-month-old rats. Once it is confirmed that there are sufficient amounts of Tau being expressed, we then check for any malfunction in the form of hyperphosphorylation. My research will be composed of analyzing the protein extracted from rat brain samples. The goal will be to determine whether Tau is being phosphorylated at specific amino acid sites. If there is significant phosphorylation at the predicted sites, then it can be said that it should mimic the pathology of Tau aggregation in neurodegeneration.