Current Trainees

Current Postdoctoral Trainees

Josef Clark
(Faculty Mentor - Rozalyn Anderson)
"RNA-based regulation of gene expression in aging and following caloric restriction."
My research is focused on how energy metabolism can influence gene expression in different tissues during aging, and in response to aging interventions such as caloric restriction (CR). Specifically, I’m interested in how the transcriptional co-activator PGC1α is regulating alternative splicing and gene expression at the co-transcriptional level in response to shifts in energy metabolism. I’m also interested in the potential role that circulating microRNAs (miRNAs) may play in consequently contributing to a metabolic CR phenotype in animals. Through these lines of investigation, I seek to better understand the molecular mechanisms of aging in the hopes we may be able create nutritional/pharmaceutical therapeutics to mimic a CR phenotype and slow the aging process.

Mark Farrugia photoMark Farrugia
(Faculty Mentor - Luigi Puglielli)
"Structural characterization and inhibition of the endoplasmic reticulum protein acetylation machinery for the purpose of ameliorating or preventing Alzheimer’s disease."
My work is focused on exploring the components of the endoplasmic reticulum acetylation machinery, namely the acetyl-CoA transporter, AT1, and the acetyltransferases, ATase1 and ATase2. In brief, my aim is to better determine the structures of these components to develop specific inhibitors for the acetyltransferases, inhibition which has been shown to halt the development of Alzheimer’s disease in a mouse model system. The main goal of this work is to determine the regulation network for endoplasmic reticulum protein acetylation and use this knowledge to allow us to better understand and control the progression of several age-related degenerative diseases.

Joshua RothJoshua Roth
(Faculty Mentor- Darryl Thelen)
"Optimal Patient-Specific Treatments for Osteoarthritis"
Symptomatic osteoarthritic is a debilitating disease that causes pain, stiffness, and loss of knee function. Symptomatic osteoarthritis of the knee occurs in 10% of men and 14% of women aged 60 years or older, and the prevalence is expected to increase with the aging population. Treatments for osteoarthritis range from non-invasive interventions (e.g., braces and shoe inserts) to invasive interventions (e.g., osteotomy and total knee replacement). The aim of my research is to investigate how both biomechanical and biological factors affect the outcome of different treatment options in these older adults. A better understanding of these factors should enable clinicians to identify the optimal treatment for an individual patient that best restores normal knee function and keeps these patients active.

Joshua RothBrian Walczak
(Faculty Mentor- Wan-Ju Li)
"Optimizing Autologous Mesenchymal Stem Cells: Preparing for the Era of Precision Medicine"
Dr. Walczak, a clinical instructor in the Department of Orthopedics and Rehabilitation, has entered the PhD CI program. He is using nanoparticles and stem cell technologies to develop novel improvements in orthopedic surgery, specifically targeting the mechanisms of aging in mesenchymal stem cells. Dr. Walczak’s background includes degrees in medicine and physical therapy. His mentor is Wan-Ju Li, PhD, Associate Professor of Biomedical Engineering and Orthopedics & Rehabilitation.

Current Predoctoral Trainees

Nicole Cummings
(Faculty Mentor - Dudley Lamming)
"The role of branched chain amino acids in metabolic health and longevity"

My work in the Lamming lab focuses on the metabolism of the branched chain amino acids (BCAAs; leucine, isoleucine, and valine). The lab found previously that restriction of dietary BCAAs reduces adiposity and improves glycemic control. We are now working to determine if restricting BCAAs can promote healthy aging and possibly extend the lifespan of several mouse models of accelerated aging. In addition, we are working on determining the mechanism by which BCAA restriction supports a healthy metabolism.

Inca DieterichInca Dieterich
(Faculty Mentor - Luigi Puglielli)
"AT-1: A critical regulator of intracellular crosstalk that ensures cellular homeostasis"

My work in Dr. Luigi Puglielli’s lab addresses questions of the aging brain at a biochemical and molecular level. Specifically: how do intracellular organelles communicate between each other to maintain cell homeostasis?  The secretory pathway is a quality control system in the cell and is responsible for acetylating nascent polypeptides in the Endoplasmic Reticulum.  AcetylCoA is the donor for aforementioned acetylation events. AT-1 is the ER membrane transporter which translocates AcetylCoA from the cytosol into the ER.  Changes in AT-1 activity are rapidly sensed by the nucleus, where it causes epigenetic changes, the mitochondria, where it causes metabolic changes, and the cytosol, where it causes changes in lipid metabolism. Therefore, AT-1 is emerging as a central novel regulator of intracellular and metabolic cross-talk linking together different cell organelles and metabolic pathways. I aim to understand the specific biochemical and molecular mechanisms that ensure this cross-talk, which are currently unknown. 

Tiaira PorterTiaira Porter
(Faculty Mentor - Darcie Moore)
"The role of nesprin-3 in mammalian neural stem cells"

Hippocampal neural stem cells (NSCs) give rise to new functional neurons throughout life in a process referred to as adult neurogenesis. With increasing age, there is a stark reduction in NSC proliferation, contributing to cognitive flexibility with mechanisms yet unclear. Disruption of the nuclear envelope has been shown to negatively affect NSC proliferation, and may be involved in regulating neurogenesis. My research is focused on characterizing nesprin-3, an outer nuclear envelope protein, in NSCs. Recently we have found that NSCs express a novel, neural-lineage specific variant of nesprin-3. The aim of my work is to characterize this isoform and its protein interactions, and determine the role it may play in NSC maintenance, and hippocampal functioning. These studies will allow us to better understand the physiological processes that govern stem cell proliferation with age.

Dylan SouderDylan Souder
(Faculty Mentor - Roz Anderson)
"Glycogen synthase kinase 3β (GSK-3β) and metabolic dysfunction in age-related neurodegeneration"

My work is characterizing the mechanisms of neuroprotection by caloric restriction (CR), a model of delayed aging.  Recently, our lab has established that CR induces a distinct state of energy metabolism in the hippocampus that is associated with reduced levels of GSK-3β, a nutrient-sensitive kinase that is known to participate in neurodegeneration.  Additionally, we have demonstrated that GSK-3β negatively regulates the activity and stability of PGC-1a, a critical regulator of energy metabolism.  We are now working to directly determine the role of GSK-3β in neuronal energy metabolism both at the cellular level, and in specific regions of the brain that are sensitive to neurodegeneration.  This will allow us to better understand the principle factors that underlie age-related cognitive impairment.

Laura SwansonLaura Swanson
(Faculty Mentor - David Wassarman)
"The Role of Aging-dependent Metabolic Dysfunction in Traumatic Brain Injury Outcomes"

Traumatic Brain Injury (TBI) is predicted to be the 3rd leading cause of death worldwide by 2020, with 50,000 victims dying each year in the United States and thousands more survivors suffering from long-term disabilities, making it one of the greatest public health burdens in society today. Elderly populations in particular are highly vulnerable to the effects of TBI, resulting in higher rates of mortality, and severe cognitive and emotional deficits in survivors. My work in the Wassarman lab utilizes our Drosophila melanogaster model of TBI to characterize how aging affects the metabolic state of flies immediately following TBI, as well as to elucidate the mechanisms that lead to disrupted energy homeostasis and ultimate TBI outcomes. These studies will provide a better understanding of the critical genes involved in metabolic dysfunction following TBI, establish where the most severe dysregulation is taking place, and identify novel targets for metabolic therapies.

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