Register for the NBAAD Symposium
The 2025 Neurobiology of Aging and Alzheimer’s Disease Symposium
- May 20
- Everett Hall (RES 100)
- Breakfast and lunch will be available
- Remote viewing via Zoom available through registration
Keynote
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“Sex-dimorphism in aging”Bérénice A. Benayoun, Ph.D. |
T32 Trainees
Luke Cooksey
DO/PhD Candidate
Cell Biology, Immunology, and Microbiology Program
Department of Microbiology, Immunology, and Genetics
Mentor: Porunelloor Mathew, PhD
Research Interests
Central nervous system cancers, cancer immunology and immunotherapy, neuro-oncology, natural killer cell immunology, neurological and neuropsychiatric pathophysiology, biomedical ethics.
Research Focus
My research currently focuses on studying immune checkpoint interactions between brain cancers and natural killer cells. The current title of my dissertation project is “Expression and Function of the csPCNA/NKp44 Immune Checkpoint in Glioblastoma.” We are studying both the expression and function of immune checkpoints in glioblastoma and medulloblastoma (and other nervous system cancers) with the eventual hopes of elucidating novel immunotherapeutic pathways to improve overall survival and overall quality-of-life for patients with brain cancer.
Sal Essajee
Physiology and Anatomy
Biomedical Science – Cardiovascular Physiology
Mentor: Johnathan Tune, Ph.D.
Research Interests
Cardiovascular disease, Valvulopathies, Vascular disease, Heart failure, Autonomic dysfunction
Research Focus
My primary research focuses on the mechanisms of onset and progression of heart failure with preserved ejection fraction (HFpEF) with specific focus on the underlying mechanisms that initiate the pathological phenotype of the disease. To date, no causal mechanistic link between an initiating insult and pathological phenotype has been determined and HFpEF has become the predominant “silent killer” of the American population. With no formal treatment modality or fundamental understanding of disease pathogenesis, HFpEF has been describes as “the greatest unmet need in cardiovascular medicine”. My doctoral research focuses on understanding the cardioprotective benefits of a Sodium-Glucose co-transporter 2 inhibitor drug, Empagliflozin which has been implicated in cardioprotection in the setting of HFpEF. By studying the potential mechanism(s) of action of the drug, we seek to obtain a better understanding of the initial insult leading to disease pathogenesis. Our lab utilizes a porcine model of heart failure and our ultimate goal is to understand the therapeutic mechanism(s) of cardioprotection conferred by Empagliflozin, to ultimately be able to better understand how hearts fail so that we may potentially prevent patients from reaching overt failure.
Viet Dinh
Physiology and Anatomy
Integrative Physiology
Mentor: Caroline A. Rickards, PhD, FAPS
Linkedin
Bluesky
Research Interests
Cerebrovascular physiology, Ischemia and hemorrhage, Brain blood flow and oxygenation
Research Focus
My research is focused on the protective effects of Pulsatile Perfusion Therapy, a novel intervention that our laboratory has developed to improve outcomes from severe blood loss and other ischemic conditions. In highly translational studies, I have demonstrated that Pulsatile Perfusion Therapy protects brain blood flow and oxygen delivery in humans during simulated hemorrhage, and also protects arterial pressure and blood flow in a rat model of severe hemorrhage. I am currently investigating the potential protection of cerebral tissue oxygen and reduction of tissue damage in the rat model and exploring the sympathetic nerve responses as a potential mechanism underlying these beneficial effects. These studies provide evidence for the potential use of Pulsatile Perfusion Therapy as a treatment for severe blood loss and other conditions of cerebral hypoperfusion.
Nathan Jones
Pharmacology & Neuroscience
College of Biomedical and Translational Sciences PhD program
Mentor: Dr. Sterling Ortega
LinkedIn
Research Interests
Traumatic Brain Injury, CD8 T-cells, Cannabidiol, Neuroinflammation
Research Focus
Traumatic brain injury (TBI) is commonly caused by car crashes, sports-related injuries, and falls, affecting millions of individuals across the globe annually. Following the initial injury, the immune system has the potential to create a neuropathogenic environment, increasing central nervous system cell death and inducing a secondary injury. My research project focuses on this TBI-induced neuroinflammation, specifically looking at CD8 T-cells. I will quantify their response to injury while analyzing their phenotype and function. I will then evaluate the therapeutic potential of cannabidiol, a non-psychoactive phytocannabinoid, hypothesizing that there will be a suppression of CD8 T-cell activity and subsequent reduction in secondary injury following cannabidiol administration. This will lead to better motor, sensory, and cognitive outcomes.
Ammar Kapic
Microbiology, Immunology, and Genetics (MIG)
Biochemistry and Cancer Biology, Traditional PhD
Mentors: Laszlo Prokai, Ph.D. and Katalin Prokai-Tatrai, Ph.D.
Linkedin
Research Interests
Age-Related Ocular Neurodegeneration, Estrogen Prodrugs, Proteomics, Phosphoproteomics, Endocrine Disruption
Research Focus
Interest in utilizing estrogens as a broad-spectrum therapeutic has re-emerged in recent years due to their beneficial pleiotropic effects, including anti-inflammatory, antioxidant, and promotion of cell survival. However, their application is limited due to their extensive peripheral side effects, which include increased cancer and blood clot risks and male feminization. My research focus is studying the therapeutic potential of the CNS-specific 17β-estradiol (E2) prodrug, 10β,17β-dihydroxyestra-1,4-dien-3-one (DHED), as a neuroprotective agent to prevent neurodegeneration of the retina and visual cortex. DHED is unique because it remains inert and does not activate the estrogen receptors unless it is converted explicitly into E2 by neuronal tissues, preventing peripheral side effects. Our robust, holistic approach utilizes mass spectrometry-based proteomic analysis alongside behavioral and histological studies to evaluate the potential neuroprotective effects of DHED-derived E2. In the future, I am interested in exploring changes in the phospho-proteome in the visual cortex and the retina to see what cell signaling pathways become dysregulated due to ocular neurodegenerative diseases such as glaucoma and whether DHED-derived E2 can ameliorate those pathways.
Rajiv Rangan
North Texas Eye Research Institute
Pharmacology and Neuroscience
Mentors: Tara Tovar-Vidales, Ph.D. & Abbot F. Clark, Ph.D.
ResearchGate
Research Interests
Glaucoma & Other Neurodegenerative Diseases, Cellular & Molecular Biology, Serotonergic Signaling, Psychedelics & Their Mechanisms of Action
Research Focus
My PhD work has largely focused on examining how serotonin may influence pro-fibrotic changes in the optic nerve head of the eye during glaucoma (a leading cause of blindness) through the use of in vitro models. Following this line of research I have investigated how the covalent modification of proteins by serotonin may influence pro-pathological changes in the eye…which has led to the obvious question of: “Can psychedelic drugs covalently modify proteins, and could this novel mechanism help explain why single doses of psychedelics exert long-lasting neurobehavioral changes?” This is what I am studying now. I’m a psychedelic researcher now. It’s not just a phase.
Savanna Smith
Integrative Physiology
College of Biomedical and Translational Sciences-Physiology and Anatomy
Mentor: Mark Cunningham Jr., Ph.D. MBA
Linkedin
Research Interests
Maternal and Fetal Health, Mitochondrial Dysfunction, Epigenetic Control of Gene Function, Hypertension, Biology of Aging, Cognitive Decline, Renal Function
Research Focus
My research is focuses on preeclamptic women and intrauterine growth restricted offspring (IUGR) as they age. These populations have an increased risk for hypertension, cognitive dysfunction, and renal function later in life. To elucidate mechanisms underlying these outcomes, we use the reduced uterine perfusion pressure (RUPP) model in Sprague Dawley Rats to produce both the preeclamptic dams and IUGR pups. This is a model that has been utilized by several other lab to induce these maternal and fetal conditions. We seek to understand how long-term disease are linked to this complicated pregnancy disorder, so that we can prevent these outcomes in the future by establishing therapeutic targets.
Kumudu Subasinghe
Department of Microbiology, Immunology & Genetics
Faculty Mentor: Nicole Phillips, Ph.D.
Degree & Discipline: Genetics
LinkedIn
Research Interests
Neurodegenerative diseases, Alzheimer’s Disease, Molecular mechanisms of Exosomes, Biomarker discovery, miRNA
Research Focus
My primary PhD research focus is to assess the biomarker potential of Neuronal enriched exosomes (NEE) in Alzheimer’s Disease (AD) by characterizing NEE and microRNA (miRNA) in longitudinal plasma samples received from the Texas Alzheimer’s Research and Care Consortium (TARCC). AD disproportionately affects Mexican Americans (MAs) due to a combination of population-specific environmental exposures and genetic risk factors. In addition to AD, Mexican Americans have a higher prevalence of metabolic comorbidities such as type 2 diabetes (T2D) that have been implicated in accelerated age-related cognitive impairment. Evidence suggests that early alterations in the AD brain can propagate to local and distal cells through the biological packages secreted by neurons called exosomes. Exosomes are a class of small, membrane-bound extracellular vesicles that mediate cell-to-cell communication through their bioactive cargo. Selective uptake of exosomes can lead to metabolic and epigenetic reprogramming in target cells. These neuronal-enriched exosomes (NEEs) cross the blood-brain barrier and thus represent an easily accessible derivative of otherwise inaccessible brain tissue in living humans. Small, non-coding RNAs known as micro RNAs (miRNA) are transcribed from nuclear DNA and function as strong intracellular expression regulators. Transported by the exosomes, they are believed to significantly alter the expression patterns of their target cells. Although many research groups have assessed NEE-bound proteins in the context of AD, miRNA cargo and the effects of NEEs on target cells remains largely unexplored. My work aims to elucidate the biological role of NEEs in order to identify novel biomarkers and targets for the design of AD interventions and diagnostic tools that will improve patient outcomes with MA population specificity.
Amanda Tucker
Cell biology, Immunology, & Genetics
College of Biomedical & Translational Sciences
Co-Mentors: Harlan Jones, Ph.D. & Nicole Phillips, Ph.D.
LinkedIn
Research Interests
Cell biology, Neurobiology, Neurodegenerative diseases, Infectious disease, Epistasis, Bioinformatics, Health disparities studies
Research Focus
My research is focused on APOE epistasis to elucidate population specific risk factors for Alzheimer’s disease. The e4 allele in the APOE gene is currently the strongest genetic risk factor for Alzheimer’s disease, and genetic risk factors for vascular diseases have been linked to genes of the renin-angiotensin-aldosterone system. Alzheimer’s disease outcomes and severity varies across racial-ethnic groups, with vascular disease and modifiable risk factors having a stronger impact on these outcomes in non-White populations. By investigating epistatic interactions between APOE and genes of the renin-angiotensin-aldosterone system, we connect genetic risk factors across diseases to elucidate epistasis as a mechanism for population specific risks of Alzheimer’s disease.
Olivia Young
Pharmacology & Neuroscience
Mentor: Denise M. Inman, PhD
LinkedIn
Research Interests
Neurodegenerative disease, Cellular metabolism, Cannabinoid signaling, Neuropharmacology, Neurobiology
Research Focus
My research focuses on the neurodegenerative diseases known together as glaucoma. I use primary astrocytes from human donors and rodents to understand the relationship of these cells at the optic nerve head. I want to understand the metabolic changes that occur in response to mechanical stress and how that contributes to glaucomatous. I am especially interested in the cannabinoid signaling system and the potential to modulate these pathways during cellular stress.
Register
NBAAD Symposium Registration
Register now for The 2025 Neurobiology of Aging and Alzheimer's Disease Symposium at The University of North Texas Health Science Center at Fort Worth.
Sponsors
- The Center for Healthy Aging
- CBTS Department of Pharmacology & Neuroscience
- T32 AG020494
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