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INTR2018FRANKLIN55390 INTR

Extinction Learning Deficits Precede Acquisition Deficits in a Mouse Model of Alzheimer’s Disease

Type: Undergraduate
Author(s): Christian Franklin Biology Julia Peterman Psychology Jordon White Psychology
Advisor(s): Michael Chumley Biology Gary Boehm Psychology Meredith Curtis Biology
Location: Session: 2; Basement; Table Number: 5

poster location

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.

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INTR2018KINSINGER59613 INTR

Reducing ROS and Chelating Metal Ions in Neuronal Cells Using Novel Compounds

Type: Undergraduate
Author(s): Olivia Kinsinger Interdisciplinary
Advisor(s): Giridhar Akkaraju Biology
Location: Session: 1; 3rd Floor; Table Number: 9

poster location

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.

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INTR2018LOPEZ34191 INTR

Reduced inflammatory response and amyloid-beta production in mice previously exposed to LPS

Type: Undergraduate
Author(s): Sofia Lopez Psychology Micah Eimerbrink Psychology Amy Hardy Biology Lauren Nakhleh Biology Kelsey Paulhus Biology Julia Peterman Psychology Morgan Thompson Biology Jordon White Psychology
Advisor(s): Gary Boehm Psychology Michael Chumley Biology Meredith Curtis Biology
Location: Session: 2; 3rd Floor; Table Number: 7

poster location

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.

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INTR2018LUCAS11885 INTR

Spark: Smart Parking for an Interconnected Campus

Type: Undergraduate
Author(s): Blake Lucas Engineering
Advisor(s): Liran Ma Computer Science
Location: Session: 1; 2nd Floor; Table Number: 9

poster location

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.

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INTR2017BARONI49831 INTR

Influence of Isolation Stress on Aβ Production and Cognitive Function in 5xFAD mice

Type: Undergraduate
Author(s): Nick Baroni Interdisciplinary Micah Eimerbrink Psychology Kelsey Paulhus Biology Julia Peterman Psychology Morgan Thompson Biology Jordon White Psychology
Advisor(s): Gary Boehm Psychology

Influence of Isolation Stress on Aβ Production and Cognitive Function in 5xFAD mice Baroni, N. J.,1 Peterman, J. L.1, White, J. D.1, Eimerbrink, M. J.1, Paulhus, K. C.2, Thompson, M. A.2, Chumley, M. J.2 & Boehm G. W.1,
1Department of Psychology, Texas Christian University
2Department of Biology, Texas Christian University
Alzheimer's Disease (AD) is a devastating neurodegenerative disease that affects nearly 44 million people worldwide, and is increasing exponentially in prevalence. Thus, research into its causes and prevention is crucial. Transgenic mouse models of Alzheimer's disease are often used to better study AD pathology. These mice have genetic mutations that result in heightened production of amyloid beta (Aβ), a pathological hallmark of AD. It has been well established that stress can influence AD pathology. This study investigates how isolation stress influences the production of amyloid beta in 5xFAD transgenic mice. In addition, we investigated whether isolation stress impacts cognition in the contextual fear conditioning (CFC) paradigm. The mice were group-housed or isolated for both 2 and 3 months, followed by cognitive testing and tissue collection. Specifically, we utilized histochemistry to examine Aβ plaque counts and an ELISA to examine soluble Aβ production. We found that isolated 5xFAD+ mice had significantly more amyloid beta plaques than group-housed animals. 5xFAD+ mice isolated for 3 months also displayed a cognitive deficit in contextual fear conditioning. All together, our results support the research that isolation stress influences Aβ production and cognitive function, and extends that to the 5xFAD transgenic mice.

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INTR2017CALCAGNO9574 INTR

Prior exposure to repeated LPS injections prevents further accumulation of hippocampal-beta-amyloid

Type: Undergraduate
Author(s): Alexa Calcagno Psychology Philip Crain Psychology Micah Eimerbrink Psychology Amy Hardy Biology Kelsey Paulhus Biology Julia Peterman Psychology Morgan Thompson Biology Jordon White Psychology
Advisor(s): Gary Boehm Psychology Michael Chumley Biology

Alzheimer’s Disease (AD) is a neurodegenerative disease currently affecting about 5.5 million Americans, and the number of people affected may rise as high as 16 million by 2050. Characteristic AD pathology of deteriorating cognitive function is correlated with neurofibrillary tangles of tau protein and Amyloid-beta (Aβ) plaques. Aβ is a peptide resulting from cleavage of the Amyloid Precursor Protein (APP) primarily present within neuronal cell membranes. The Aβ peptide can be cleaved at different lengths, but Aβ1-42 is the most neurotoxic. Aβ1-42 primarily aggregates in the hippocampus, where it further stimulates the release of cytokine proteins initiating an inflammatory response. Previous studies in our lab have shown that short-term inflammation induced by injection of lipopolysaccharide (LPS) leads to an inflammatory response that stimulates production of Aβ1-42 peptides. The goal of this project was to determine whether this effect could be exacerbated through a second injection series of LPS after a fourteen-day recovery interval, thus modeling multiple, independent, bacterial infections, like that seen in humans. The animals were given 7 days of 250 mg/kg LPS or saline injections, a two-week break, and another 7 days of LPS or saline. Contrary to what was predicted, Aβ levels were not potentiated. This effect was found to be related to decreased inflammatory response upon secondary administration of LPS, as IL-1β mRNA was significantly lower in the group that got two rounds of LPS. Current studies of our lab are evaluating whether these results are related to the presence of antibodies to LPS or a specific tolerance mechanism.

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INTR2017NGUYEN65117 INTR

An IoT-based Real Time Low Cost Monitoring and Notification System for Aged Care

Type: Undergraduate
Author(s): Quang Nguyen Computer Science
Advisor(s): Sue Gong Physics & Astronomy Liran Ma Computer Science

The challenge of taking care of aged patients who lost control of their bladders and bowel movements is to respond to the patients’ needs in a timely manner, which often requires a caretaker (e.g. a family member or a hired assistant) to stay on watch 24/7. In light of advance in cloud computing, we present a real-time low-cost monitoring and notification system that can continuously monitor the patients bedding condition, detect the conditions that help is needed and notify the care-takers. The system consists of TI SensorTags, Raspberry Pis, and IBM Bluemix. The TI SensorTag is a sensing device, while Raspberry Pi acts as a messenger receiving data collected by TI SensorTags via Bluetooth technology and transmitting the data to Bluemix, a cloud-based platform developed by IBM, via WiFi.

The system frequently senses bedding conditions of patients. Data is uploaded to a server residing on IBM Cloud, which processes data and sends appropriate notifications. The availability of cloud technology and small signal processing units, as well as advance in sensor technologies, allow us to build a low-cost system that can help caregivers address the patients’ needs effectively. As a result, the quality of care for patients is improved.

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