Alzheimer’s disease (AD) is a progressive brain disorder and the most common form of dementia. The disease gradually destroys brain cells, leading to confusion, erratic behavior, and severe loss of memory. Alzheimer’s is eventually fatal, and no treatment or cure has been discovered. Researchers aim to better understand Alzheimer’s pathology through the use of a transgenic mouse model of AD, the 5xFAD mice. A previous study by Bonardi et al. (2011) has shown that another model of AD, the APP/PS1 mouse, exhibits a deficit in extinction learning before it displays a deficit in acquisition. We aim to determine if this same trend exists in 5xFAD mice, despite having more extensive genetic mutations. Learning will be assessed using the Contextual Fear Conditioning (CFC) paradigm, where the mice are introduced to an environmental context and experience a mild aversive stimulus. When reintroduced to the context 24 hours later, mice will freeze if they acquired a memory for the pairing of an aversive stimulus with the novel context. Freezing is an instinctive rodent fear response. After repeated trials of exposure to the environment in the absence of an aversive stimulus, the mice gradually freeze less. This is indicative of new learning of the environment no longer being paired with the stimulus, or extinction of the initial association. The 5xFAD mice typically exhibit impaired acquisition by 6 months of age as compared to wild type mice. The present study examined if the 5xFAD mice would display a deficit in extinction learning prior to this deficit in acquisition. Preliminary data indicate that 5xFAD mice, like APP/PS1 mice, show a deficit in memory extinction before they exhibit a loss of memory acquisition. Three-month old FAD mice extinguish more slowly than three-month old wild type mice, but show no difference in acquisition. This research is important because it indicates alternative cognitive measures may allow for earlier diagnosis of neurodegenerative diseases, such as AD.

It is estimated that 45% of people over the age of 85 in the U.S. suffer from Alzheimer’s disease. Patients with Alzheimer’s disease, which is characterized by cognitive deficiencies and memory loss, have higher concentrations of amyloid plaques in brain tissue than patients without the disease. Abnormal levels of transition metal ions Fe, Zn, and Cu in brain tissue are associated with amyloid beta plaques and also have been shown to catalyze the generation of excess reactive oxygen species (ROS) and cause oxidative stress. The combination of the ROS generation and the amyloid plaque formation results in neurodegeneration, which ultimately causes the memory loss and ultimate death associated with Alzheimer’s. We have synthesized the compounds L2 and L4 which are designed to be chelating agents of metal ions and also scavengers of ROS. We hypothesize that due to their chelating properties and pyridol groups, L2 and L4 should reduce oxidative damage in neuronal cells by chelating metal ions and scavenging radicals. Furthermore, we hypothesize that due to its extra pyridol group, L4 will be a stronger antioxidant than L2. The cytotoxicity of the compounds was tested on HT-22 neuronal cells. Neuronal cells will be treated with BSO, a compound that induces formation of ROS, in the presence and absence of L2 and L4. If our hypothesis is correct, our compounds should reduce the oxidative damage induced by BSO, and L4 should be more effective at doing so than L2.

Alzheimer’s disease (AD) is a neurodegenerative condition in which beta-amyloid protein accumulates into plaques, and tau protein forms neurofibrillary tangles. In the past, our laboratory has shown that repeated inflammatory events increase beta-amyloid in the hippocampus of male C57BL6/J mice. We sought to determine the effect of a second exposure to the bacterial mimetic lipopolysaccharide (LPS) on beta amyloid accumulation. An initial round of seven, once daily LPS or sterile saline injections, was administered to male C57BL6/J adult mice. Fourteen days after the last injection, a second round of LPS or saline injections was given, followed by tissue collection and quantification of beta-amyloid levels in the hippocampus. The results showed that animals injected with two rounds of LPS had significantly lower levels of beta-amyloid accumulation than those animals injected with just a single round of LPS, although both groups had significantly higher levels of beta-amyloid than the saline control animals. These results suggest a reduced inflammatory response following a secondary exposure to LPS. More specifically, animals exposed to LPS for a second time showed significantly less central and peripheral inflammation four hours after LPS administration than animals with no prior exposure. In addition, increased levels of IgM and IgG were discovered in the mice with prior LPS exposure. This could indicate possible antibody production against LPS or beta-amyloid rather than tolerance of the LPS as a mechanism for the reduced inflammatory response. In order to establish whether this results in a life-long effect, we are currently exploring the impact of LPS administration in old age for mice who were exposed to LPS earlier in life.

With the increasing student population trend at TCU, parking on campus is equally increasing
in difficulty. Due to the limited campus space, expanding parking availability is not a feasible
solution. Spark is a smart parking system that monitors the status of each space in parking lots,
indicating the space’s occupancy status on an aerial “Google Maps” view of the parking lot in a
smartphone application and, potentially, a website. The application could be linked to the TCU
Single-Sign-On for increased security and to make it easier for TCU students, faculty, and staff
to save their parking preferences. Spark can measure the fill rate of individual lots, recommend
a time-to-leave to procure a parking spot, and even provide update notifications on the status
of the user’s preferred lots.

Understanding of the wound healing process can be used to make more tailor-made medicine and to determine the nature of this healing process. In this research we use MATLAB software along with the ADI method to solve a partial differential equation that models wound healing by treating keratin as a diffusion process. A significant hurdle to overcome is finding the appropriate initial conditions, that is to accurately extract boundary data from photos taken with different equipment, lighting, or resolution.