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Current PhD Students

jenders

Jonathan Enders
j255e970@kumc.edu

Peripheral diabetic neuropathy is among the most common complications of diabetes, greatly reducing quality of life and resulting in altered sensation, pain, and numbness. Methylglyoxal is a metabolite upregulated in diabetic patients with neuropathy and has been shown to cause pain and contribute to other peripheral neuropathies; however, therapies aimed at scavenging methylglyoxal have largely failed in clinic. Previous work from our lab demonstrates that a ketogenic diet is effective in rescuing neuropathy in models of diabetes and prediabetes. Recently, we observed decreased circulating methylglyoxal in mice fed a ketogenic diet. Our overall goal is to identify how a ketogenic diet contributes to methylglyoxal scavenging in peripheral diabetic neuropathy.

JFrick

Jenna Frick 
jfrick3@kumc.edu

Self-Fellow

Exposure to stress early in life has been associated with adult-onset comorbidities including chronic pain, obesity-related metabolic disorder, and physical inactivity. Altered regulation of the hypothalamic-pituitary-adrenal (HPA) axis has been linked to these syndromes; however, the underlying mechanism that links these disorders together remains unknown. Previous data has shown that a high-fat/high-sucrose diet exacerbates outcomes induced by early life stress such as increased fat mass and mechanical allodynia. Our overall goal is to identify the underlying mechanisms for increased weight gain and sensitivity associated with stress and diet. 

agabrielli

Alexander Gabrielli
a228g039@kumc.edu

Alzheimer's disease is the leading cause of dementia-a progressive and insidious decline in cognitive function that typically manifests in older age. As populations across the globe continue to age, Alzheimer's increasingly presents a significant challenge for society in both economic and human costs. The molecular and genetic origins of Alzheimer's disease remain both complex and elusive. However, evidence increasingly suggests an important role for mitochondrial dysfunction, metabolism, and failure of the respiratory chain in the early pathogenesis of the disease. Neuroblastoma cells subjected to respiratory stress through chronic mitochondrial DNA depletion resemble the aging brain in many ways, particularly the metabolic and respiratory profile that accompanies dementia-associated brain aging. Interestingly, these mitochondrial DNA-depleted cells exhibit profoundly increased production and secretion of apolipoprotein E (apoE), a protein involved in lipoprotein formation and lipid shuttling. In the CNS, apoE appears to be involved in amyloid precursor protein transcription and amyloid beta secretion, among other roles. A variant of the APOE gene, ε4, is the leading genetic risk factor in late-onset Alzheimer's disease, which is the most common subset. Why this upregulation of apoE occurs in response to chronic mitochondrial injury is not clear. My research aims to clarify the mechanisms underlying this phenomenon, in hopes of yielding new insights into the role of apoE in responding to mitochondrial dysfunction and the attendant stressors. Understanding these mechanisms may elucidate the role of apoE in Alzheimer's neurodegeneration.

zgreen

Zachary Green
zgreen@kumc.edu

A growing body of evidence suggests prescribed exercise regimens can result in cognitive benefits in Alzheimer's Diseases patients, potentially due to the acute exercise response inducing changes in permeating factors of the brain. While the acute exercise response has been studied in young, healthy individuals, little is known about it in Alzheimer's Disease. My focus is on linking metabolic changes owed to the acute exercise response with structural and functional measures of brain activity in hopes of elucidating the mechanisms behind the apparent cognitive benefit of exercise in the Alzheimer's brain.

bjones

Brittni Jones                                                                          bjones17@kumc.edu

A rise in the national rate of child maltreatment as well as prolonged NICU stays for premature babies to survive at early gestational ages both contribute to an increased rate of childhood adversity and stress. Early life stress predisposes individuals to both mental illnesses and chronic pain disorders later in life, but mechanisms and early interventions are yet to be understood. We utilize neonatal maternal separation in mice to model early life stress. In humans, exercise reduces perceptions of pain as well as depression and anxiety. Therefore, mice have access to voluntary exercise wheels in order to study exercise's ability to attenuate the negative affects of early life stress by measuring changes in neurogenesis in the dentate gyrus as well as the impact of DNA methylation on stress-specific genes. 

bmenta1

Blaise Menta
bmenta@kumc.edu

The role of mitochondrial dysfunction in neurological disorders, has gained greater interest in recent years. Mitochondria synthesize fatty acids that are crucial for the production of ATP. I am investigating how perturbations in mitochondrial fatty acid synthesis (mtFAS) influence energy production and how alterations in bioenergetic homeostasis affect cells in the central nervous system.

rstair

Rena Stair
rstair2@kumc.edu

Self-Fellow

Uncovering the genetic and epigenetic contributors to the manifestation and maintenance of pain. 

Adam Willits
awillits@kumc.edu 

Irritable Bowel Syndrome and the associated functional abdominal pain are common diagnoses that have no known cause. The few available treatments include altering gut motility to reduce IBS symptoms, but these interventions have no effect on abdominal pain. Since familial studies have shown the heritability of IBS, our main goal is to uncover how gene expression changes in the colon and surrounding tissues may contribute to IBS susceptibility. Not only could these genetic factors answer questions about disease pathology, but they may also provide potential drug target candidates for IBS-associated abdominal pain.

Last modified: May 13, 2021
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