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Current Trainees

Photo Name Project Mentor Email
Knopp, Rachel Dysfunction of calcium homeostasis is widely reported to contribute to synaptic degeneration in AD. This imbalance leads to the hyper-activation of two cysteine proteases: calpain-1 and cathepsin B. The over-activation of these proteases have been proposed as underlying contributors not only to AD, but also to traumatic brain injury (TBI) and ischemic stroke (IS). The goal of this research is to determine an optimal strategy for targeting these proteases in treatment of neurodegenerative disorders, while also further elucidating the mechanisms by which they contribute to AD. Greg Thatcher, Ph.D. rknopp3@uic.edu
Karstens, Aimee We are quantifying plasma lipoprotein profiles using size exclusion chromatography in the context of a Mediterranean Diet intervention to improve cognition in female obese older adults, and additionally examining the effect of APOE4, the greatest genetic risk for Alzheimer’s Disease, on the efficacy of the the intervention (i.e., improving cognition and plasma lipoprotein profiles). The plasma lipoprotein profile is established by the elution of the lipoproteins from a size exclusion column, with the larger, lipid-laden chylomicrons and very low density lipoproteins eluting first, followed by low density lipoproteins, high density lipoprotein (HDL)-2, HDL-3, and then free protein. Using the fractions fast protein liquid chromatography, we can further quantify lipids (e.g., cholesterol) and other particles (e.g., oligomeric amyloid beta). Mary Jo LaDu, Ph.D. and Scott Langenecker Ph.D. karsten2@uic.edu
Lewandowski, Cutler We aim to identify and develop tissue-selective ABCA1 agonists (TSAAgs) as Alzheimer's Disease (AD) drug candidates with multifactorial therapeutic potential. We are utilizing medicinal chemistry approaches to synthesize novel lead TSAAgs based on chemotypes that have been identified and validated in a high-throughput screen. Lead TSAAgs will undergo extensive evaluation in vitro, followed by in vivo testing in healthy mice to establish pharmacodynamic and pharmacokinetic profiles and in two preclinical disease models to assess their potential as AD therapeutics for progression into human clinical trials. Greg Thatcher, Ph.D. lewando4@uic.edu
Morrissey, Zachery I will be using resting-state functional magnetic resonance imaging (rs-fMRI) to study the connectome changes that occur in transgenic mouse models of Alzheimer's Disease (AD) and neurogenesis. By using molecular biology techniques in conjunction with emerging neuroimaging analysis methods, we can better understand the cellular and neural network mechanisms underlying neurodegeneration. These experiments will give a system-level insight into how brain connectomes are altered as a result of AD, and improve our clinical understanding of how cognition improves as a result of environmental enrichment and neurogenesis. Alex Leow, MD/Ph.D. and Orly Lazarov, Ph.D. zmorri4@uic.edu

Previous Trainees

Photo Name Project Mentor Email
Bonds, Jacqueline There are several risk factors that contribute to the development of Alzheimer's disease (AD), including insulin resistance and type 2 diabetes (T2D). According to data collected from the Mayo Clinic Alzheimer's Disease Registry, more than 80% of AD cases also present with either T2D or an impaired glucose metabolism disorder. Unfortunately, the mechanisms underlying the link between these two diseases is complex and very poorly understood. This project aims to clarify how deficits in caveolin-1 expression in the brain causes AD-related neuropathology and compromised neurogenesis. Orly Lazarov, Ph.D. and Jacob Haus, Ph.D. jbonds3@uic.edu
Lee, Sue Recent reports have linked traumatic brain injury (TBI) ranging from sport athlete's concussions to soldier blast impacts to earlier onset dementia. Still the link between mild trauma and its role in the ability to deplete a person's "cognitive reserve" as they age leading to dementia is still unknown. The proposed research seeks to 1) characterize a novel mouse model of aging, Aldh2-/-, induced with either single or repetitive mTBI, 2) identify and visualize lipid distribution changes on brain slices of these mice with MALDI imaging mass spectrometry, and 3) utilize computational and MRI neuroimaging techniques to identify mechanisms that may lead to identification of underlying mechanisms or early biomarkers that lead to increased risk of dementia. We hypothesize that by better understanding the long-term negative consequences of TBI from different perspectives will allow us to develop treatments for ADRD with prior mTBI. Greg Thatcher, Ph.D. and Stephanie Cologma, Ph.D. suelee1@uic.edu